Name: balloon-based injury to induce myointimal hyperplasia in the mouse abdominal aorta
Uploaded: 2018-02-07T12:30:00.000+00:00
Duration: 7 min 32 s
Description: Watch this Scientific Journal Video about Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta at JoVE.com

Los autores agradecen a Christiane Pahrmann para su asistencia técnica.
D.W. fue apoyado por el Max Kade Foundation. T.D. recibidas becas de la Fundación de Kröner otro (2012_EKES.04) y la Deutsche Forschungsgemeinschaft (DE2133/2-1_. S. S. recibió becas de investigación de la Deutsche Forschungsgemeinschaft (DFG; SCHR992/3-1, SCHR992/4-1).

Animales recibieron atención humanitaria conforme a la guía de principios de los animales de laboratorio, prepararon por el Instituto de recursos de animales laboratorio y publicaron por los institutos nacionales de salud. Animales todos los protocolos fueron aprobados por la autoridad local responsable ('' Amt für Gesundheit und Verbraucherschutz, Hansestadt (Oficina de salud y protección del consumidor) Hamburgo '').
1. preparación de catéter
Nota: Consulte la Tabla de materiales para obtener información sobre el catéter.
<ol><li>Tomar el catéter del soporte del catéter.</li>
	<li>Tire de la guía de la luz a través del orificio distal hacia fuera.</li>
	<li>Poner en una gota de cianoacrilato en el extremo distal del catéter. PRECAUCIÓN: Use guantes de látex o nitrilo.</li>
	<li>Coloque la guía en el puerto de RX del catéter y avanzarlo a través del lumen hasta el puerto distal. Luego, tire la guía ligeramente para dejar un espacio de ~ 5 m m hasta el final.</li>
	<li>Espere 5 minutos para permitir que el adhesivo se seque.</li>
	<li>Mueva la guía, debe ser fijo. Si es aún móvil, repita los pasos 1.3-1.6.</li>
	<li>Llene una jeringa de 3 mL con solución salina al de 0.9% 1.5 mL y conéctelo en el puerto de inflado del globo.</li>
	<li>Empuje el émbolo de la jeringa para comprobar la inflación del globo. Salir de 0.6 mL solución salina en la jeringa.</li>
</ol>2. preparación de Mouse
<ol><li>Obtener ratones machos a la edad de 14 semanas aproximadamente 30 g de peso. Nota: Se utilizaron animales obtenidos desde el Instituto de animales de laboratorio. Aquí utilizamos el C57BL/6J.</li>
	<li>Utilizar una cámara de inducción para anestesiar el ratón con 2.0-2.5% isofurane (tasa de flujo de oxígeno de 500 mL/min).</li>
	<li>Coloque el ratón sobre su espalda en un cojín de calefacción y mantener la anestesia con una máscara que cubre la boca y la nariz del ratón. Si hay suficiente profundidad de la anestesia por pellizcar las patas traseras y la cola para verificar la ausencia de los reflejos.</li>
	<li>Eliminar el vello abdominal utilizando un cortador de pelo.</li>
	<li>Extiende las piernas traseras y fijar su posición con cinta.</li>
	<li>Desinfectar la zona abdominal con povidona-yodo, seguido de etanol al 80%. Repita este paso dos veces más.</li>
	<li>Utilice un paño quirúrgico para asegurarse no contaminado Haz sitio quirúrgico. Abrir las capas de piel y músculo a lo largo de la linea alba con una tijera (o bisturí) para exponer los órganos abdominales.</li>
	<li>Poner los intestinos en un guante hidratada solución salina 0.9% y envolver para mantenerlos húmedos.</li>
	<li>Use dos pinzas finas para quitar el tejido fino graso por encima de la aorta abdominal.</li>
	<li>Utilizando una jeringa de insulina (30G), inyectar 250 μl de solución de heparina (50 U/mL) en la Vena Cava Inferior (IVC) y espere 3 minutos para su distribución sistémica. Heparina se suprimen la hemostasia y prevenir la coagulación no deseada durante la cirugía.</li>
	<li>Utilizando dos pinzas, disecar la aorta del infrarenal hasta su bifurcación y sus vasos de rama saliente.</li>
	<li>Ligar los vasos laterales, que deben colocarse en la zona sujeta, con un cauterizador de alta temperatura.</li>
	<li>Detener el flujo de sangre por pinzamiento de la aorta del infrarenal directamente debajo de las arterias renales.</li>
	<li>Coloque la segunda abrazadera en una posición distal justo por encima de la bifurcación aórtica.</li>
	<li>Realizar una pequeña incisión horizontal con unas tijeras en el punto medio entre las abrazaderas a lo largo de la nave. Nota: El tamaño de la incisión debe ser equivalente a 1/3 de la circunferencia del vaso.</li>
	<li>Inserte una jeringa con una aguja (30G) en la incisión y al ras de la aorta con solución de heparina de 250 μl (50 U/mL).</li>
	<li>Utilizando suturas 10-0, coloque un nudo a cada lado de la incisión.</li>
	<li>Dilatación de la aorta por inserción de un dilatador de vasos en la incisión y extendió el vaso ligeramente. Repetir la dilatación 2 a 3 veces.</li>
	<li>Hidratar el catéter de balón con solución salina al 0.9%.</li>
	<li>Inserte el catéter de globo aplanado en la aorta y avanzar hacia la pinza proximal en la aorta.</li>
	<li>Al llegar a la pinza proximal, cuidadosamente abra la pinza proximal e inflar el balón para evitar fugas de sangre, inyectando ~0.6 mL de solución salina. Nota: La relación entre el globo inflado al recipiente es 1.5:1.</li>
	<li>Haga avanzar el catéter retrógrado de aproximadamente 2 cm.</li>
	<li>Tire el catéter ampliado, al desinflar el balón ligeramente por la liberación de la jeringa.</li>
	<li>Vuelva a colocar la pinza proximal cuando el catéter alcanza la incisión de la aorta. Desinflar el balón completamente y sáquela.</li>
	<li>Enjuague la aorta con solución de heparina de 250 μl (50 U/mL) usando una jeringa de 30G.</li>
	<li>Cerrar la incisión aórtica usando suturas 10-0. Lugar interrumpe puntadas en cada lado lateral, seguido por una o dos puntadas en el lado ventral.</li>
	<li>Abra la pinza distal. En caso de sangrado, vuelva a cerrar la pinza y colocar puntos de sutura adicionales.</li>
	<li>Abrir con cuidado la pinza proximal.</li>
	<li>Coloque dos hisopos en la sutura para apoyarlo y detener cualquier sangrado.</li>
	<li>Colocar pinzas hemostáticas absorbibles sobre la sutura para mantenerla. Nota: Un pulso aórtico debe ser visible distal de la incisión.</li>
	<li>Coloque los intestinos en el abdomen.</li>
	<li>Lavar la cavidad abdominal con solución salina 0.9% estéril, que ha sido precalentado a 37 ° C.</li>
	<li>Cerrar la capa de músculo abdominal usando suturas corrientes 6-0.</li>
	<li>Cierre la piel con suturas corrientes 5-0.</li>
	<li>Inyectar en forma subcutánea 4-5 mg/kg de carprofeno antes de permitir que el ratón despertar. Seguimiento del animal hasta que se ha ganado conciencia, mantener recumbency esternal. No el animal solo en una jaula hasta su recuperación completa.</li>
	<li>Añadir químicos al agua de bebida (50 mg/100 mL) como medicamento para el dolor por 3 días y monitorear diariamente el animal. Generalmente ratones como el dulce sabor de Metamizol y comenzar a beber inmediatamente después de la cirugía. Si lo prefiere, pueden utilizarse agentes inyectables de liberación sostenida en lugar de químicos. Nota: El período de observación para este modelo es de 28 días.</li>
</ol>3. histopatología
<ol><li>La cosecha la aorta lesionado globo después de 28 días preparando los ratones como se describe en los pasos 2.2 a 2.9.</li>
	<li>Utilice tijeras para quitar la aorta lesión de globo (entre la bifurcación y 0,3 mm por encima de los vasos renales) y eutanasia el ratón cortando a su corazón.</li>
	<li>Irrigue el lumen del vaso con 0.9% NaCl.</li>
	<li>Fijar la embarcación cosechada en paraformaldehído al 4% (PFA) durante la noche y deshidratar en el aumento de las concentraciones de etanol, a partir de etanol al 70% de etanol al 80% durante 1 hora, 2 horas, etanol al 95% durante 2 horas y el etanol al 100% durante 5 horas. Luego, incubar las muestras en xileno durante 2 horas 3 veces, antes de infiltrarse en las muestras con parafina. Nota: en lugar de rubor el buque cosechado con 0.9% NaCl, puede aclararse con 4% PFA. PRECAUCIÓN: PFA y el xileno son tóxicos y deben manipularse con especial cuidado.</li>
	<li>Embeber la muestra en parafina y cortadas en rodajas de 5 μm de espesor utilizando un micrótomo.</li>
	<li>Desparafinizar el portaobjetos con xileno 3 veces durante 5 minutos.</li>
	<li>Rehidratar las diapositivas de tejidos utilizando una serie decreciente de etanol. Iniciar con 100% etanol 2 veces durante 5 min, seguido de 3 minutos de etanol 95%, 80% y 70%.</li>
	<li>Mancha de los portaobjetos con tinción tricrómica de Masson como descrito18.</li>
	<li>Deshidratar diapositivas manchadas en etanol al 100% 2 veces por 10 minutos cada uno. Claro con xileno 2 veces de 10 minutos cada uno y Monte en medio de montaje.</li>
	<li>Ver las diapositivas con un microscopio de campo brillante. Utilizar un objetivo con 5 aumentos y una apertura numérica de 0.12 para un cuadro de resumen o una lente de 20 aumentos x con una apertura numérica de 0.35 para observación detallada.</li>
</ol>4. microscopia de la inmunofluorescencia de
<ol><li>Rehidratar las diapositivas de tejidos utilizando una serie decreciente de etanol. Iniciar con 100% etanol 2 veces durante 5 min, seguido de 3 minutos de etanol 95%, 80% y 70%.</li>
	<li>Realizar recuperación de antígeno por calentar los portaobjetos en solución de recuperación de antígeno en un vapor durante 20 minutos.</li>
	<li>Deje que las diapositivas se enfríe a temperatura ambiente.</li>
	<li>Después de lavar los portaobjetos tres veces con tampón fosfato salino (PBS), aplicar solución de bloqueo de antígeno en secciones de 30 minutos.</li>
	<li>Lave el portaobjetos tres veces durante 5 minutos con PBS.</li>
	<li>Incubar las secciones con anticuerpo primario diluido en un diluyente de anticuerpo primario. Nota: El momento de concentración y la incubación debe ser elegido por separado para cada anticuerpo.</li>
	<li>Lave el portaobjetos tres veces durante 5 minutos con PBS para retirar el anticuerpo no Unido.</li>
	<li>Incubar las secciones con un anticuerpo secundario conjugado previamente diluido en un diluyente de anticuerpo secundario. Nota: El momento de concentración y la incubación debe ser elegido por separado para cada anticuerpo.</li>
	<li>Eliminar los anticuerpos no Unidos por el lavado de los portaobjetos durante 5 minutos tres veces.</li>
	<li>Contratinción los núcleos celulares con 4', 6-diamidino-2-phenylindole (DAPI) durante 15 minutos; la concentración final de DAPI debe ser 350 nM.</li>
	<li>Montar diapositivas en inmunofluorescencia compatible con solución de montaje. Nota: Usando la solución de montaje incorrecto puede oscurecer la señal de fluorescencia.</li>
	<li>Diapositivas de la vista con un microscopio de fluorescencia. Use un lente de aumento de 40 x con una apertura numérica de 1.3.</li>
</ol>

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Los autores no tienen nada que revelar.

Este artículo demuestra un modelo murino para el desarrollo de la hiperplasia myointimal y permite la exploración de los procesos patológicos subyacentes y la prueba de nuevos medicamentos o terapéuticas.
El paso más crítico en este protocolo es la denudación de la aorta. Debe prestarse especial cuidado durante este paso como denudación excesiva dará lugar a la formación de aneurismas y el fracaso del modelo. Por otro lado, si la denudación se realiza escaso, desarrollará myointima...

Estenosis arterial en las arterias coronarias y periféricas tiene un gran efecto sobre la morbilidad y la mortalidad de pacientes1. Un mecanismo patológico subyacente es la hiperplasia myointima (MH), que se caracteriza por aumento de la proliferación, migración y síntesis de matriz extracelular proteínas del músculo liso vascular células (SMC)2. SMC se encuentran en la capa media del vaso y migrar sobre el estímulo a la superficie de la luz. Señales estimulantes incluyen factores de crecimiento, citoquinas, contacto célula-célula, lípidos, componentes de la matriz extracelular y esquileo mecánico y estiran las fuerzas3,4,5,6. Lesiones de la pared del vaso, patológica o iatrogénica, causan la célula endotelial y daño a las células del músculo liso y estimulan reacciones inflamatorias y así llevan a MH7.
Diferentes modelos animales están disponibles para el estudio de lesión arterial y la hiperplasia myointima. Grandes animales como cerdos o perros tienen la ventaja de compartir una similar de la arteria y la anatomía coronaria con los seres humanos y son especialmente adecuados para estudios investigando técnicas, procedimiento y dispositivos de angioplastia8. Sin embargo, modelos de cerdo tienen el inconveniente de mayor trombogenicidad9,10, mientras que los perros sólo tienen una suave respuesta a lesiones de vasos11. Además, todos los modelos animales grandes requieren especial, equipos y personal, que está relacionado con altos costos y no siempre está disponibles en una institución. Modelos animales pequeños incluyen ratas y ratones. En comparación con las ratas, ratones tienen las ventajas de menor costo y la existencia de una variedad de golpes modelos. El modelo descrito en este video se puede combinar con ApoE-/-los ratones alimentados con una dieta occidental que mímico de cerca el ajuste clínico de la angioplastia en los vasos ateroscleróticos12. Los modelos anteriores inducida por lesión vascular vía cable lesión13, desecación líquido14, primavera15o manguito lesiones16. Puesto que la naturaleza de la lesión afectará grandemente el desarrollo y Constitución de MH, utilizando un catéter con balón para inducir lesión de vaso es la mejor manera de imitar el ajuste clínico.
En este artículo describimos un nuevo método para inducir a MH con un catéter con balón en ratones. El uso de un catéter con balón (1,2 mm x 6 mm) con un puerto de RX (figura 1A) permite el raspado de la capa íntima y, al mismo tiempo, la inducción de un overdistension del buque. Ambos de estos factores son importantes factores desencadenantes para el desarrollo de MH. El tiempo de observación para este modelo es de 28 días17.

<table><tbody><tr><td>10-0 Ethilon suture</td><td>Ethicon</td><td>2814G</td><td></td></tr><tr><td>3 mL Syringe</td><td>BD Medical</td><td>309658</td><td></td></tr><tr><td>37% HCl</td><td>Sigma-Aldrich</td><td>H1758</td><td></td></tr><tr><td>5-0 prolene suture</td><td>Ethicon</td><td>EH7229H</td><td></td></tr><tr><td>6-0 prolene suture</td><td>Ethicon</td><td>8706H</td><td></td></tr><tr><td>Acid Fuchsin</td><td>Sigma-Aldrich</td><td>F8129-25G</td><td>Trichrome staining</td></tr><tr><td>Antigen retrieval solution</td><td>Dako</td><td>S1699</td><td></td></tr><tr><td>Azophloxin</td><td>Waldeck</td><td>1B-103</td><td>Trichrome staining</td></tr><tr><td>Bepanthen Eye and Nose ointment</td><td>Bayer</td><td>1578675</td><td>Eye ointment</td></tr><tr><td>Betadine Solution</td><td>Betadine Purdue Pharma</td><td>NDC:67618-152</td><td></td></tr><tr><td>C57BL/6J</td><td>Charles River</td><td>Stock number 000664</td><td></td></tr><tr><td>Clamp applicator</td><td>Fine Science Tools</td><td>18056-14</td><td>JAW DIMS: 4 x 0.75 mm
LENGTH: 13 mm</td></tr><tr><td>Collagen 3</td><td>abcam</td><td>ab7778</td><td>Antibody</td></tr><tr><td>DAPI</td><td>Thermo Fischer</td><td>D1306</td><td></td></tr><tr><td>Donkey anti-Goat IgG AF555</td><td>Invitrogen</td><td>A21432</td><td>Secondary antibody</td></tr><tr><td>Donkey anti-Rabbit IgG AF488</td><td>Invitrogen</td><td>A21206</td><td>Secondary antibody</td></tr><tr><td>Donkey anti-Rabbit IgG AF488</td><td>Invitrogen</td><td>A11055</td><td>Secondary antibody</td></tr><tr><td>Donkey anti-Rabbit IgG AF555</td><td>Invitrogen</td><td>A31572</td><td>Secondary antibody</td></tr><tr><td>Ethanol 70%</td><td>Th. Geyer</td><td>2270</td><td></td></tr><tr><td>Ethanol 96%</td><td>Th. Geyer</td><td>2295</td><td></td></tr><tr><td>Ethanol absolute</td><td>Th. Geyer</td><td>2246</td><td></td></tr><tr><td>FAP</td><td>abcam</td><td>ab28246</td><td>Antibody</td></tr><tr><td>Forceps fine</td><td>Fine Science Tools</td><td>11251-20</td><td></td></tr><tr><td>Forceps standard</td><td>Fine Science Tools</td><td>11023-10</td><td></td></tr><tr><td>Glacial Acetic Acid</td><td>Sigma-Aldrich</td><td>537020</td><td></td></tr><tr><td>Hair clipper</td><td>WAHL</td><td>8786-451A ARCO SE</td><td></td></tr><tr><td>Heparin</td><td>Rotexmedica</td><td>PZN 3862340</td><td>25.000 I.E./mL</td></tr><tr><td>High temperature cautery kit</td><td>Bovie</td><td>18010-00</td><td></td></tr><tr><td>Image-iT FX Signal Enhancer</td><td>Invitrogen</td><td>I36933</td><td>Blocking solution</td></tr><tr><td>Light Green SF</td><td>Waldeck</td><td>1B-211</td><td>Trichrome staining</td></tr><tr><td>Microsurgical clamp</td><td>Fine Science Tools</td><td>18055-04</td><td>Micro-Serrefine - 4mm</td></tr><tr><td>MINI TREK Coronary Dilatation Catheter 1.20 mm x 6 mm / Rapid-Exchange</td><td>Abbott</td><td>1012268-06U</td><td></td></tr><tr><td>Molybdatophosphoric acid hydrate</td><td>Merck</td><td>1.00532.0100</td><td>Trichrome staining</td></tr><tr><td>NaCl 0,9%</td><td>B.Braun</td><td>PZN 06063042 Art. Nr.: 3570160</td><td></td></tr><tr><td>Needle holder</td><td>Fine Science Tools</td><td>12075-14</td><td></td></tr><tr><td>Novaminsulfon</td><td>Ratiopharm</td><td>PZN 03530402</td><td>Metamizole</td></tr><tr><td>Orange G</td><td>Waldeck</td><td>1B-221</td><td>Trichrome staining</td></tr><tr><td>Paraffin</td><td>Leica biosystems</td><td>REF 39602004</td><td></td></tr><tr><td>PBS pH 7,4</td><td>Gibco</td><td>10010023</td><td></td></tr><tr><td>PFA 4%</td><td>Electron Microscopy Sciences</td><td>#157135S</td><td></td></tr><tr><td>Ponceau S solution</td><td>Serva Electrophoresis</td><td>33427</td><td>Trichrome staining</td></tr><tr><td>Primary antibody diluent</td><td>Dako</td><td>S3022</td><td></td></tr><tr><td>Prolong Gold Mounting solution</td><td>Thermo Fischer</td><td>P36930</td><td>Mounting solution for immunofluorescence stained slides</td></tr><tr><td>Replaceable Fine Tip</td><td>Bovie</td><td>H101</td><td></td></tr><tr><td>Resorcin-Fuchsin Weigert</td><td>Waldeck</td><td>2E-30</td><td>Trichrome staining</td></tr><tr><td>Rimadyl</td><td>Pfizer</td><td>400684.00.00</td><td>Carprofen</td></tr><tr><td>Scissors</td><td>Fine Science Tools</td><td>14028-10</td><td></td></tr><tr><td>Scissors Vannas-style</td><td>Fine Science Tools</td><td>15000-03</td><td></td></tr><tr><td>Secondary antibody diluent</td><td>Dako</td><td>S0809</td><td></td></tr><tr><td>Fast acting Adhesive MINIS 3x1g</td><td>UHU</td><td>45370</td><td>Cyanoacrylate</td></tr><tr><td>Slide Rack</td><td>Ted Pella</td><td>21057</td><td></td></tr><tr><td>SM22</td><td>abcam</td><td>ab10135</td><td>Antibody</td></tr><tr><td>SMA</td><td>abcam</td><td>ab21027</td><td>Antibody</td></tr><tr><td>Staining dish</td><td>Ted Pella</td><td>21075</td><td></td></tr><tr><td>Surgical microscope</td><td>Leica</td><td>M651</td><td></td></tr><tr><td>Tabotamp fibrillar</td><td>Ethicon</td><td>431962</td><td>Absorbable hemostat</td></tr><tr><td>Transpore Surgical Tape</td><td>3M</td><td>1527-1</td><td></td></tr><tr><td>U-100 Insulin syringe</td><td>BD Medical</td><td>324825</td><td></td></tr><tr><td>Vessel Dilator</td><td>Fine Science Tools</td><td>18603-14</td><td></td></tr><tr><td>Vitro-Clud</td><td>Langenbrinck</td><td>04-0001</td><td></td></tr><tr><td>Weigerts iron hematoxylin Kit</td><td>Merck</td><td>1.15973.0002</td><td>Trichrome staining</td></tr><tr><td>Xylene</td><td>Th. Geyer</td><td>3410</td><td></td></tr></tbody></table>

balloon-based injury to induce myointimal hyperplasia in the mouse abdominal aorta

El uso de modelos animales es esencial para una mejor comprensión de la MH, una de las principales causas de estenosis arterial. En este artículo, nos muestran un modelo de denudación murine del globo, que es comparable con modelos de lesión de buque establecido en grandes animales. El modelo de denudación de aorta con catéteres de balón imita el ajuste clínico y conduce a cambios fisiológicos y pathobiological comparables. Brevemente, después de realizar una incisión horizontal en la aorta abdominalis, un catéter con balón se introduce en el recipiente, inflado y se introdujo retrogradely. Inflación del balón dará lugar a lesiones de la íntima y overdistension del buque. Después de retirar el catéter, se cerrará la incisión aórtica con puntos de sutura únicas. El modelo mostrado en este artículo es reproducible, fácil de realizar y pueden establecerse de forma rápida y fiable. Es especialmente conveniente para la evaluación de agentes terapéuticos experimentales costosos, que pueden aplicarse de una manera económica. Mediante el uso de diferentes cepas de ratón knockout, podrá evaluarse el impacto de diferentes genes en el desarrollo de MH.

Denudación de globo es un modelo adecuado para estudiar el desarrollo de MH en ratones. Animales recuperan bien de la cirugía y mostrar después de la operación de una excelente condición física. Se estableció este modelo en 50 ratones con menos de 3% de mortalidad debido a la intervención quirúrgica. Figuras 1B -C muestra los principales pasos quirúrgicos. Después de una incisión en la piel a lo largo de la linea alba, id...

Watch this Scientific Journal Video about Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta at JoVE.com

Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

Este artículo demuestra un modelo murino para el desarrollo de la hiperplasia myointimal (MH) después de lesión de globo.

Lesión basada en globo para inducir la hiperplasia Myointimal de la Aorta Abdominal de ratón

The use of animal models is essential for a better understanding of MH, one major cause for arterial stenosis.In this article, we demonstrate a murine ...

balloon-based-injury-to-induce-myointimal-hyperplasia-mouse-abdominal

Universidad de Cartagena UDEC

Research

JoVE Journal

Medicine

9.5K vistas.  University Heart Center. Este artículo demuestra un modelo murino para el desarrollo de la hiperplasia myointimal (MH) después de lesión de globo.

Video: Balloon-based Injury to Induce Myointimal Hyperplasia in the Mouse Abdominal Aorta

Inducing Myointimal Hyperplasia Versus Atherosclerosis in Mice: An Introduction of Two Valid Models

Various in vivo laboratory rodent models for the induction of artery stenosis have been established to mimic diseases that include arterial plaque formation and stenosis, as observed for example in ischemic heart disease. Two highly reproducible mouse models&#160;&#8211;&#160;both resulting in artery stenosis but each underlying a different pathway of development&#160;&#8211; are introduced here. The models represent the two most common causes of artery stenosis; namely one mouse model for each myointimal hyperplasia, and atherosclerosis are shown. To induce myointimal hyperplasia, a balloon catheter injury of the abdominal aorta is performed. For the development of atherosclerotic plaque, the ApoE -/- mouse model in combination with western fatty diet is used. Different model-adapted options for the measurement and evaluation of the results are named and described in this manuscript. The introduction and comparison of these two models provides information for scientists to choose the appropriate artery stenosis model in accordance to the scientific question asked.

This video shows two models of intimal plaque development in murine arteries and emphasizes the differences in myointimal hyperplasia and atherosclerosis.

Inducir miointimal Hiperplasia Versus aterosclerosis en ratones: una introducción de dos modelos válidos

Various in vivo laboratory rodent models for the induction of artery stenosis have been established to mimic diseases that include arterial plaque ...

Investigación

Medicina

Vascular Balloon Injury and Intraluminal Administration in Rat Carotid Artery

The carotid artery balloon injury model in rats has been well established for over two decades. It remains an important method to study the molecular and cellular mechanisms involved in vascular smooth muscle dedifferentiation, neointima formation and vascular remodeling. Male Sprague-Dawley rats are the most frequently employed animals for this model. Female rats are not preferred as female hormones are protective against vascular diseases and thus introduce a variation into this procedure. The left carotid is typically injured with the right carotid serving as a negative control. Left carotid injury is caused by the inflated balloon that denudes the endothelium and distends the vessel wall. Following injury, potential therapeutic strategies such as the use of pharmacological compounds and either gene or shRNA transfer can be evaluated. Typically for gene or shRNA transfer, the injured section of the vessel lumen is locally transduced for 30 min with viral particles encoding either a protein or shRNA for delivery and expression in the injured vessel wall. Neointimal thickening representing proliferative vascular smooth muscle cells usually peaks at 2 weeks after injury. Vessels are mostly harvested at this time point for cellular and molecular analysis of cell signaling pathways as well as gene and protein expression. Vessels can also be harvested at earlier time points to determine the onset of expression and/or activation of a specific protein or pathway, depending on the experimental aims intended. Vessels can be characterized and evaluated using histological staining, immunohistochemistry, protein/mRNA assays, and activity assays. The intact right carotid artery from the same animal is an ideal internal control. Injury-induced changes in molecular and cellular parameters can be evaluated by comparing the injured artery to the internal right control artery. Likewise, therapeutic modalities can be evaluated by comparing the injured and treated artery to the control injured only artery.

This protocol uses a balloon catheter to cause an intraluminal injury on the rat carotid artery and henceforth elicit neointimal hyperplasia. This is a well-established model for studying the mechanisms of vascular remodeling in response to injury. It is also widely used to determine the validity of potential therapeutic approaches.

Lesión Vascular Globo y Administración intraluminal en rata arteria carótida

The carotid artery balloon injury model in rats has been well established for over two decades. It remains an important method to study the molecular and ...

A Murine Model of Arterial Restenosis: Technical Aspects of Femoral Wire Injury

Cardiovascular disease caused by atherosclerosis is the leading cause of death in the developed world. Narrowing of the vessel lumen, due to atherosclerotic plaque development or the rupturing of established plaques, interrupts normal blood flow leading to various morbidities such as myocardial infarction and stroke. In the clinic endovascular procedures such as angioplasty are commonly performed to reopen the lumen. However, these treatments inevitably damage the vessel wall as well as the vascular endothelium, triggering an excessive healing response and the development of a neointimal plaque that extends into the lumen causing vessel restenosis (re-narrowing). Restenosis remains a major cause of failure of endovascular treatments for atherosclerosis. Thus, preclinical animal models of restenosis are vitally important for investigating the pathophysiological mechanisms as well as translational approaches to vascular interventions. Among several murine experimental models, femoral artery wire injury is widely accepted as the most suitable for studies of post-angioplasty restenosis because it closely resembles the angioplasty procedure that injures both endothelium and vessel wall. However, many researchers have difficulty utilizing this model due to its high degree of technical difficulty. This is primarily because a metal wire needs to be inserted into the femoral artery, which is approximately three times thinner than the wire, to generate sufficient injury to induce prominent neointima. Here, we describe the essential surgical details to effectively overcome the major technical difficulties of this model. By following the presented procedures, performing the mouse femoral artery wire injury becomes easier. Once familiarized, the whole procedure can be completed within 20 min.

The mouse femoral artery wire injury model of restenosis is technically challenging. In this protocol we show the key technical details essential for successfully performing wire injury to induce consistent&#160;neointima for studies of restenosis.

Un modelo murino de restenosis arterial: Aspectos Técnicos del femoral Lesiones alambre

Cardiovascular disease caused by atherosclerosis is the leading cause of death in the developed world. Narrowing of the vessel lumen, due to ...

Induction of Accelerated Atherosclerosis in Mice: The "Wire-Injury" Model

Atherosclerosis is a proliferative fibro-inflammatory disease developing in the arterial wall, inducing a deficient blood flow or a lack of blood flow. Moreover, by rupture of the defective vascular wall, atherosclerosis induces occlusive thrombus formation, which represents the main cause of myocardial infarction or stroke and the most frequent cause of death. Despite the advances in the cardiovascular field, many questions remain unanswered, and additional basic research is essential to improve our understanding of the molecular mechanisms during atherosclerosis and its effects. Due to limited clinical studies, there is a need for representative animal models recreating atherosclerotic conditions such as neointima formation after stent implantation, balloon angioplasty, or endarterectomy. Since the mouse presents many advantages and is the most frequently used model for studying molecular processes, the current study proposes an invasive procedure of endothelial denudation, also known as the wire-injury model, which is representative of the human condition of neointima formation in arteries after revascularization procedures.

This study describes an invasive procedure for the induction of accelerated atherosclerosis in mice. In comparison to other methods using electric- or cryo-induced injury, mechanical-induced injury mimics the human condition of restenosis after revascularization therapies and is ideal for the study of the molecular mechanisms involved.

Inducción de la Aterosclerosis Acelerada en Ratones: El Modelo de "Lesiones por Alambre"

Atherosclerosis is a proliferative fibro-inflammatory disease developing in the arterial wall, inducing a deficient blood flow or a lack of blood flow. ...

Reproducible Arterial Denudation Injury by Infrarenal Abdominal Aortic Clamping in a Murine Model

Percutaneous vascular interventions uniformly result in arterial denudation injuries that subsequently lead to thrombosis and restenosis. These complications can be attributed to impairments in re-endothelialization within the wound margins. Yet, the cellular and molecular mechanisms of re-endothelialization remain to be defined. While several animal models to study re-endothelialization after arterial denudation are available, few are performed in the mouse because of surgical limitations. This undermines the opportunity to exploit transgenic mouse lines and investigate the contribution of specific genes to the process of re-endothelialization. Here, we present a step-by-step protocol for creating a highly reproducible murine model of arterial denudation injury in the infrarenal abdominal aorta using external vascular clamping. Immunocytochemical staining of injured aortas for fibrinogen and &#946;-catenin demonstrate the exposure of a pro-thrombotic surface and the border of intact endothelium, respectively. The method presented here has the advantages of speed, excellent overall survival rate, and relative technical ease, creating a uniquely practical tool for imposing arterial denudation injury in transgenic mouse models. Using this method, investigators may elucidate the mechanisms of re-endothelialization under normal or pathological conditions.

Understanding the cellular and molecular mechanisms of re-endothelialization following arterial denudation injury is of paramount importance in preventing thrombosis and restenosis of arteries. Here we describe a protocol for reproducible arterial denudation injury of the infrarenal abdominal aorta. The procedure was developed to investigate the underlying mechanisms that regulate endothelial regeneration using mouse models.

Reproducible lesión arterial Denudación por pinzamiento aórtico abdominal infrarrenal en un modelo murino

Percutaneous vascular interventions uniformly result in arterial denudation injuries that subsequently lead to thrombosis and restenosis. These ...

The Rabbit Model of Accelerated Atherosclerosis: A Methodological Perspective of the Iliac Artery Balloon Injury

Acute coronary syndrome resulting from coronary occlusion following atherosclerotic plaque development and rupture is the leading cause of death in the industrialized world. New Zealand White (NZW) rabbits are widely used as an animal model for the study of atherosclerosis. They develop spontaneous lesions when fed with atherogenic diet; however, this requires long time of 4 - 8 months. To further enhance and accelerate atherogenesis, a combination of atherogenic diet and mechanical endothelial injury is often employed. The presented procedure for inducing atherosclerotic plaques in rabbits uses a balloon catheter to disrupt the endothelium in the left iliac artery of NZW rabbits fed with atherogenic diet. Such mechanical damage caused by the balloon catheter induces a chain of inflammatory reactions initiating neointimal lipid accumulation in a time dependent fashion. Atherosclerotic plaque following balloon injury show neointimal thickening with extensive lipid infiltration, high smooth muscle cell content and presence of macrophage derived foam cells. This technique is simple, reproducible and produces plaque of controlled length within the iliac artery. The whole procedure is completed within 20 - 30 min. The procedure is safe with low mortality and also offers high success in obtaining substantial intimal lesions. The procedure of balloon catheter induced arterial injury results in atherosclerosis within two weeks. This model can be used for investigating the disease pathology, diagnostic imaging and to evaluate new therapeutic strategies.

Animal models of atherosclerosis are essential to understand the mechanism and to investigate newer approaches to prevent plaque development or rupture, a leading cause of death in the industrialized world. This protocol uses a combination of balloon injury and cholesterol rich diet to induce atherosclerotic plaques in rabbit iliac artery.

El modelo de conejo de ateroesclerosis acelerada: una perspectiva metodológica de la lesión de globo de la arteria ilíaca

Acute coronary syndrome resulting from coronary occlusion following atherosclerotic plaque development and rupture is the leading cause of death in the ...

A Rat Carotid Artery Pressure-Controlled Segmental Balloon Injury with Periadventitial Therapeutic Application

Cardiovascular disease remains the leading cause of death and disability worldwide, in part due to atherosclerosis. Atherosclerotic plaque narrows the luminal surface area in arteries thereby reducing adequate blood flow to organs and distal tissues. Clinically, revascularization procedures such as balloon angioplasty with or without stent placement aim to restore blood flow. Although these procedures reestablish blood flow by reducing plaque burden, they damage the vessel wall, which initiates the arterial healing response. The prolonged healing response causes arterial restenosis, or re-narrowing, ultimately limiting the long-term success of these revascularization procedures. Therefore, preclinical animal models are integral for analyzing the pathophysiological mechanisms driving restenosis, and provide the opportunity to test novel therapeutic strategies. Murine models are cheaper and easier to operate on than large animal models. Balloon or wire injury are the two commonly accepted injury modalities used in murine models. Balloon injury models in particular mimic the clinical angioplasty procedure and cause adequate damage to the artery for the development of restenosis. Herein we describe the surgical details for performing and histologically analyzing the modified, pressure-controlled rat carotid artery balloon injury model. Additionally, this protocol highlights how local periadventitial application of therapeutics can be used to inhibit neointimal hyperplasia. Lastly, we present light sheet fluorescence microscopy as a novel approach for imaging and visualizing the arterial injury in three-dimensions.

The rat carotid artery balloon injury mimics the clinical angioplasty procedure performed to restore blood flow in atherosclerotic vessels. This model induces the arterial injury response by distending the arterial wall, and denuding the intimal layer of endothelial cells, ultimately causing remodeling and an intimal hyperplastic response.

Una lesión de globo segmentario controlada por presión arterial carótida de rata con aplicación terapéutica periavential

Cardiovascular disease remains the leading cause of death and disability worldwide, in part due to atherosclerosis. Atherosclerotic plaque narrows the ...

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Arterial reconstruction, whether angioplasty or bypass surgery, involves iatrogenic trauma causing endothelial disruption and vascular smooth muscle cell (VSMC) proliferation. Common murine models study small vessels such as the carotid and femoral arteries. Herein we describe an in vivo system in which both VSMC proliferation and endothelial barrier function can be simultaneously assessed in a large vessel. We studied the infrarenal aortic response to injury in C57BL/6 mice. The aorta was injured from the left renal vein to the aortic bifurcation by 30 transmural crushes of 5-seconds duration with a cotton-tipped applicator. Morphological changes were assessed with conventional histology. Aorta wall thickness was measured from the luminal surface to the adventitia. EdU integration and counter staining with DAPI and alpha-actin was used to demonstrate VSMC proliferation. Activation of ERK1/2, a known moderator of intimal hyperplasia formation, was determined by Western Blot analysis. The effect of inflammation was determined by immunohistochemistry for B-cells, T-cells, and macrophages. En face sections of endothelium were visualized with scanning electron microscopy (SEM). Endothelial barrier function was determined with Evans Blue staining. Transmural injury resulted in aortic wall thickening. This injury induced VSMC proliferation, most prominently at 3 days after injury, and early activation of ERK1/2 and decreased p27kip1 expression. Injury did not result in increased B-cells, T-cells, or macrophages infiltration in the vessel wall. Injury caused partial endothelial cell denudation and loss of cell-cell contact. Injury resulted in a significant loss of endothelial barrier function, which returned to baseline after seven days. The murine transmural blunt aortic injury model provides an efficient system to simultaneously study both VSMC proliferation and endothelial barrier function in a large vessel.

Murine Aortic Crush Injury: An Efficient In Vivo Model of Smooth Muscle Cell Proliferation and Endothelial Function

Restenosis following cardiovascular procedures (bypass surgery, angioplasty, or stenting) is a significant problem reducing the durability of these procedures. An ideal therapy would inhibit smooth muscle cell (VSMC) proliferation while promoting regeneration of the endothelium. We describe a model for simultaneous assessment of VSMC proliferation and endothelial function in vivo.

Lesión por aplastamiento aórtico murino: una eficacia<em&gt; In Vivo</em&gt; Modelo de proliferación de células musculares lisas y función endotelial

Arterial reconstruction, whether angioplasty or bypass surgery, involves iatrogenic trauma causing endothelial disruption and vascular smooth muscle cell ...

Biología

<meta charset="utf8"></head><body>Investigación de los mecanismos moleculares que subyacen al aneurisma de aorta abdominal murino

A Mouse Abdominal Aortic Aneurysm Model by Periadventitial Calcium Chloride and Elastase Infiltration

Abdominal aortic aneurysm (AAA) is a life-threatening disease associated with high mortality rates. It is characterized by the permanent dilation of the abdominal aorta with at least a 50% increase in arterial diameter. Various animal models of AAA have been introduced to mimic the pathophysiological changes and study the underlying mechanisms of AAA. Among these models, the calcium chloride (CaCl2)- and elastase-induced AAA models are commonly used in mice. However, these methods have certain limitations. Traditional intraluminal porcine pancreatic elastase (PPE) perfusion is associated with high technical difficulty and a high rupture rate, while periadventitial administration of PPE yields inconsistent results. In addition, the CaCl2-induced AAA model lacks human AAA features, such as atherothrombosis and aneurysm rupture. Therefore, the combined application of CaCl2 and PPE has been proposed as an approach to enhance success rates and induce greater diameter increases in AAA animal models. This manuscript presents a comprehensive protocol for establishing a mouse AAA model through periaortic infiltration of PPE and CaCl2 in the infrarenal segment of the abdominal aorta. By following this protocol, we can achieve an AAA formation rate of approximately 90% with technical simplicity and reproducibility. Further ultrasound and histological experiments confirm that this model effectively replicates the morphological and pathological changes observed in human AAA.

<meta charset="utf8"></head><body>Autor destacado: Desarrollo y caracterización de un modelo de ratón para el aneurisma de aorta abdominal

This manuscript presents a protocol for establishing a mouse abdominal aortic aneurysm model using calcium chloride and elastase, combining the advantages of previous modeling methods. This model can be utilized to investigate the pathophysiological mechanisms underlying abdominal aortic aneurysms.

Un modelo de aneurisma de aorta abdominal de ratón por infiltración periadventicial de cloruro de calcio y elastasa

Abdominal aortic aneurysm (AAA) is a life-threatening disease associated with high mortality rates. It is characterized by the permanent dilation of the ...

Lesión basada en globo para inducir la hiperplasia Myointimal de la Aorta Abdominal de ratón

Resumen

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