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

Os autores Christiane Pahrmann agradecer a assistência técnica.
D.W. foi apoiado por Max Kade Foundation. T.D. recebido concede a outra Kröner Fondation (2012_EKES.04) e a Deutsche Forschungsgemeinschaft (DE2133/2-1. _. Bolsas de investigação S. S. recebeu o Deutsche Forschungsgemeinschaft (DFG; SCHR992/3-1, SCHR992/4-1).

Os animais receberam atendimento humano em conformidade com o guia para os princípios de animais de laboratório, preparado pelo Instituto de recursos animais de laboratório e publicado pela National Institutes of Health. Todos os protocolos de animais foram aprovados pela autoridade local competente (' Amt für Gesundheit und Verbraucherschutz, (serviço de saúde e defesa do consumidor) de Hansestadt Hamburg ').
1. cateter preparação
Nota: Consulte a Tabela de materiais , para obter informações sobre o cateter.
<ol><li>Retire o cateter o titular do cateter.</li>
	<li>Puxe o fio-guia do lúmen através do orifício distal para fora.</li>
	<li>Colocar em uma gota de adesivo de cianoacrilato na extremidade distal do cateter. Cuidado: Use luvas de látex ou nitrilo.</li>
	<li>Coloque o fio-guia na porta RX do cateter e avançá-lo através do lúmen para o porto distal. Depois, puxe o fio-guia ligeiramente para deixar um espaço de ~ 5 mm até o fim.</li>
	<li>Espere 5 minutos para permitir que o adesivo secar.</li>
	<li>Mover o fio-guia, deve ser fixado. Se é ainda móvel, repita os passos 1.3-1.6.</li>
	<li>Encher uma seringa de 3 mL com soro fisiológico a 0,9% 1,5 mL e conectá-lo à porta de insuflação do balão.</li>
	<li>Empurre o êmbolo da seringa para teste de insuflação do balão. Deixe 0,6 mL de soro fisiológico na seringa.</li>
</ol>2. preparação do rato
<ol><li>Obter camundongos machos na idade de 14 semanas, pesando aproximadamente 30 g. Nota: Usamos animais obtidos a partir do Instituto de animais de laboratório. Aqui usamos C57BL/6J.</li>
	<li>Use uma câmara de indução para anestesiar o mouse com isofurane de 2.0-2.5% (taxa de fluxo de oxigênio de 500 mL/min).</li>
	<li>Coloque o mouse sobre as costas de uma almofada de aquecimento e manter anestesia com uma máscara cobrindo a boca e o nariz do mouse. Verifique se há suficiente profundidade da anestesia beliscar as patas e cauda para verificar a ausência de reflexos.</li>
	<li>Remova o cabelo abdominal usando uma máquina de cortar cabelo.</li>
	<li>Espalhe as patas traseiras e fixar sua posição usando a fita.</li>
	<li>Desinfete a área abdominal usando iodo-povidona, seguido por 80% de etanol. Repita mais duas vezes.</li>
	<li>Use um pano cirúrgico para garantir local cirúrgico não ser contaminado. Abra as camadas de pele e músculo ao longo da linea alba com uma tesoura (ou bisturi) para expor os órgãos abdominais.</li>
	<li>Colocar os intestinos em uma luva de hidratada salina 0,9% e enrole para mantê-los húmida.</li>
	<li>Use dois pinça fina para remover o tecido adiposo acima a aorta abdominal.</li>
	<li>Usando uma seringa de insulina (30G), injetar 250 µ l de solução de heparina (50 U/mL) para a veia Cava Inferior (VCI) e espere 3 min para sua distribuição sistêmica. Heparina poderá suprimir a hemostasia e evitar coagulação indesejada durante a cirurgia.</li>
	<li>Usando duas pinças, disse a aorta infra-renal até sua bifurcação e seus vasos de ramo a saída.</li>
	<li>Ligar os vasos colaterais, que são esperados para ser colocado na área do preso, com um cauterizador de alta temperatura.</li>
	<li>Interromper o fluxo de sangue, fixando a aorta infra-renal diretamente abaixo das artérias renais.</li>
	<li>Coloque uma segunda pinça em uma posição distal logo acima da bifurcação da aorta.</li>
	<li>Realize uma pequena incisão horizontal usando a tesoura no ponto médio entre os grampos ao longo do navio. Nota: O tamanho da incisão deve ser equivalente a 1/3 da circunferência do vaso.</li>
	<li>Introduza uma seringa com uma agulha (30G) da incisão e liberar a aorta com 250 µ l de solução heparina (50 U/mL).</li>
	<li>Utilizar suturas de 10-0, coloque um único nó de cada lado da incisão.</li>
	<li>Dilatação da aorta inserindo um dilatador de vaso a incisão e espalhar o recipiente ligeiramente. Repita a dilatação de 2 a 3 vezes.</li>
	<li>Hidrate o cateter-balão com soro fisiológico a 0,9%.</li>
	<li>Insira o cateter-balão achatado na aorta e avançá-lo em direção a pinça proximal na aorta.</li>
	<li>Quando chegar a pinça proximal, cuidadosamente Abra a pinça proximal e insuflar o balão para evitar o vazamento de sangue, através da injeção de ~0.6 mL de solução salina. Nota: A relação do balão inflado de navio é 1.5: 1.</li>
	<li>Avance o cateter retrógrado para aproximadamente 2 cm.</li>
	<li>Puxe o cateter expandido, enquanto desinflar o balão ligeiramente liberando a seringa.</li>
	<li>Quando o cateter chega a incisão da aorta, recolocar a pinça proximal. Esvazie o balão completamente e removê-lo.</li>
	<li>Enxágue a aorta com 250 µ l de solução heparina (50 U/mL), utilizando uma seringa de 30G.</li>
	<li>Feche a incisão da aorta usando suturas de 10-0. Lugar interrompido pontos de cada lado lateral, seguido por um ou dois pontos no lado ventral.</li>
	<li>Abra a pinça distal. Em caso de sangramento, fechar a pinça novamente e colocar pontos adicionais.</li>
	<li>Abra a pinça proximal com cuidado.</li>
	<li>Coloque dois cotonetes na sutura para apoiá-lo e parar qualquer sangramento.</li>
	<li>Coloque hemostatos absorvíveis na sutura para sustentá-lo. Nota: Um pulso aórtico deve ser visível distal da incisão.</li>
	<li>Coloque os intestinos para o abdômen.</li>
	<li>Enxaguar a cavidade abdominal com solução salina 0,9%, que foi previamente aquecido a 37 ° C.</li>
	<li>Feche a camada muscular abdominal usando suturas execução de 6-0.</li>
	<li>Feche a pele com suturas de execução de 5-0.</li>
	<li>Injete o carprofeno de 4-5 mg/kg por via subcutânea antes de permitir que o mouse para acordar. Monitorar o animal até ganhou consciência, manter a prostração esternal. Manter o animal em uma gaiola até recuperação completa.</li>
	<li>Adicionar o metamizol à água potável (50 mg/100 mL) como medicação para a dor por 3 dias e monitorar o animal diariamente. Geralmente os ratos como o doce sabor de dipirona e começam a beber imediatamente após a cirurgia. Se preferirem, agentes injetáveis de liberação sustentada podem ser usados em vez de dipirona. Nota: O período de observação para este modelo é de 28 dias.</li>
</ol>3. histopatologia
<ol><li>Colheita da aorta com balão-ferido depois de 28 dias, preparando os ratos como descrito nos passos 2.2 a 2.9.</li>
	<li>Use a tesoura para remover a balão-ferido da aorta (entre a bifurcação e 0,3 mm acima dos vasos renais) e eutanásia o mouse cortando seu coração.</li>
	<li>Irrigue o lúmen do vaso com 0,9% NaCl.</li>
	<li>Consertar o navio colhido em paraformaldeído 4% (PFA) durante a noite e desidratá-lo em concentrações crescentes de etanol, começando com etanol a 70% por 2 horas, 80% de etanol por 1 hora, etanol 95% por 2 horas e 100% de etanol por 5 horas. Então, Incube as amostras em xilol durante 2 horas 3 vezes, antes de me infiltrar as amostras com parafina. Nota: em vez de liberar o navio colhido com 0,9% NaCl, ele pode ser liberado com 4% PFA. Cuidado: PFA e xileno são tóxicos e devem ser manuseados com cuidado especial.</li>
	<li>Incorporar a amostra em parafina e cortados em fatias de espessura de 5 µm usando um micrótomo.</li>
	<li>Deparaffinize os slides com xileno 3 vezes durante 5 minutos.</li>
	<li>Reidratar slides de tecido usando uma série decrescente de etanol. Comece com 100% de etanol 2 vezes por 5 min, seguido de 3 minutos de etanol 95%, 80% e 70%.</li>
	<li>Mancha os slides com coloração tricromo de Masson como descrito18.</li>
	<li>Desidrate corrediças manchadas em etanol 100% 2 vezes por 10 min cada. Limpar com xilol 2 vezes por 10 min cada e montar no meio de montagem.</li>
	<li>Visualizar os slides com um microscópio de campo claro. Use uma lente com 5x ampliação e uma abertura numérica de 0,12 por imagens uma visão ou uma lente com 20 ampliações de x com uma abertura numérica de 0.35 para observação detalhada.</li>
</ol>4. microscopia de imunofluorescência
<ol><li>Reidratar slides de tecido usando uma série decrescente de etanol. Comece com 100% de etanol 2 vezes por 5 min, seguido por 3 min de etanol 95%, 80% e 70%.</li>
	<li>Execute recuperação de antígeno aquecendo as lâminas em solução de recuperação do antígeno em um navio a vapor por 20 min.</li>
	<li>Deixe arrefecer o slides até à temperatura.</li>
	<li>Depois de lavar os slides por três vezes com solução salina tamponada fosfato (PBS), aplica solução de bloqueio de antígeno em seções por 30 min.</li>
	<li>Lave slides três vezes por 5 min com PBS.</li>
	<li>Incube as seções com anticorpo primário diluído em diluente de anticorpo primário. Nota: O momento de concentração e a incubação deve ser escolhido separadamente para cada anticorpo.</li>
	<li>Lave slides três vezes por 5 min com PBS para remover anticorpos não acoplado.</li>
	<li>Incube as seções com um anticorpo secundário conjugado previamente diluído em diluente de anticorpo secundário. Nota: O momento de concentração e a incubação deve ser escolhido separadamente para cada anticorpo.</li>
	<li>Remova anticorpos desacoplados lavando os slides por 5 min, três vezes.</li>
	<li>Counterstain os núcleos de célula usando 4', 6-diamidino-2-phenylindole (DAPI) por 15 min; a concentração final de DAPI deve ser de 350 nM.</li>
	<li>Monte as lâminas na imunofluorescência compatível com solução de montagem. Nota: Usando a solução de montagem errada pode obscurecer o sinal de fluorescência.</li>
	<li>Exibição de slides com um microscópio de fluorescência. Use uma lente de ampliação de 40x com uma abertura numérica de 1.3.</li>
</ol>

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Este artigo demonstra um modelo murino para estudar o desenvolvimento de hiperplasia myointimal e permite a exploração dos processos patológicos subjacentes e os testes de novas drogas ou opções terapêuticas.
O passo mais crítico neste protocolo é o desnudamento da aorta. Cuidado especial deve ser dada durante esta etapa como denudação excessiva conduzirá à formação de aneurisma e fracasso do modelo. Por outro lado, se a denudação é executada insuficientemente, myointima muito...

Estenose arterial nas artérias coronárias e periféricas tem um grande efeito sobre a morbidade e mortalidade de pacientes1. Um mecanismo patológico subjacente é hiperplasia myointima (MH), que é caracterizada pelo aumento da proliferação, migração e síntese de proteínas da matriz extracelular do músculo liso vascular células (SMC)2. SMC estão localizados na camada de mídia do navio e migrar a estimulação para a superfície do lúmen. Sinais estimulatórios incluem fatores de crescimento, citocinas, contato célula-célula, lipídeos, componentes de matriz extracelular e cisalhamento mecânico e estendem as forças3,4,5,6. Lesões da parede do vaso, patológica ou iatrogênica, causam células endoteliais e danos nas células musculares lisas e estimulam reações inflamatórias e assim levam a MH7.
Diferentes modelos animais estão atualmente disponíveis para estudar a lesão arterial e hiperplasia myointima. Grandes animais como porcos ou cães têm a vantagem de compartilhar uma artéria semelhante e anatomia coronariana com seres humanos e são especialmente adequados para estudos investigando angioplastia dispositivos, procedimento e técnicas8. No entanto, modelos de porco têm a desvantagem da maior trombogenicidade9,10, enquanto os cães só têm uma resposta suave ao navio lesão11. Além disso, todos os grandes modelos animais exigem especial habitação, equipamentos e funcionários, que estão conectados com custos elevados e não estão sempre disponíveis na instituição. Pequenos modelos animais incluem ratos e camundongos. Em comparação com ratos, os ratos têm as vantagens de custo mais baixo e a existência de uma variedade de nocaute do modelos. O modelo descrito neste vídeo pode ser combinado com ApoE-/-os ratos alimentados com uma dieta ocidental pròxima imitar o ambiente clínico de angioplastia em vasos aterosclerótica12. Modelos anteriores induzido por lesão vascular via fio lesão13, fluido dessecação14, Primavera15ou de lesão do manguito16. Desde que a natureza da lesão afetará grandemente o desenvolvimento e a constituição de MH, utilizar um cateter balão para induzir lesões no vaso é a melhor maneira para imitar o ambiente clínico.
Neste artigo nós descrevemos um método novo para induzir MH com um cateter de balão em camundongos. O uso de um cateter balão (1,2 x 6 mm) com um RX-Port (figura 1A) permite a raspagem da camada da íntima e, ao mesmo tempo, a indução de uma hiperdistensão do navio. Ambos esses fatores são gatilhos importantes para o desenvolvimento do MH. O tempo de observação para este modelo é de 28 dias17.

<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

O uso de modelos animais é essencial para uma melhor compreensão do MH, uma das principais causas de estenose arterial. Neste artigo, vamos demonstrar um modelo de denudação murino de balão, que é comparável com os modelos de lesão navio estabelecido em animais de grandes porte. O modelo de desnudamento de aorta com cateteres balão imita o ambiente clínico e leva a mudanças fisiológicas e pathobiological comparáveis. Brevemente, após a realização de uma incisão horizontal na aorta abdominalis, um cateter balão será inserido dentro do vaso sanguíneo, inflado e introduziu retrogradely. Inflação do balão vai levar a lesão da íntima e hiperdistensão do navio. Depois de retirar o cateter, a incisão da aorta será fechada com pontos simples. O modelo mostrado neste artigo é reprodutível, fácil de realizar e pode ser estabelecida de forma rápida e confiável. É especialmente apropriado para avaliar caros agentes terapêuticos experimentais, que podem ser aplicados de forma econômica. Usando diferentes cepas de mata-mata-rato, pode ser avaliado o impacto de diferentes genes no desenvolvimento do MH.

Desnudamento do balão é um modelo adequado para estudar o desenvolvimento de MH em camundongos. Animais recuperar bem da cirurgia e mostram uma pós-operação condição física excelente. Nós estabelecemos este modelo em 50 ratos com menos de 3% de mortalidade devido a procedimento cirúrgico. Figuras 1B -C mostrar as principais etapas cirúrgicas. Após uma incisão de pele ao longo do linea alba, identificar a aorta abdomi...

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 artigo demonstra um modelo murino para estudar o desenvolvimento de hiperplasia myointimal (MH) após lesão aórtica balão.

Lesão baseada no balão para induzir a hiperplasia Myointimal da Aorta Abdominal de Mouse

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 visualizações.  University Heart Center. Este artigo demonstra um modelo murino para estudar o desenvolvimento de hiperplasia myointimal (MH) após lesão aórtica balão.

Vídeo: 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.

Induzir miointimais Hiperplasia Versus aterosclerose em camundongos: uma introdução de dois modelos válidos

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

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.

Lesão Balloon Vascular e Administração Intraluminal em Rat 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.

Um modelo murino de Arterial Restenosis: Aspectos Técnicos do Femoral Injury Fio

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.

Indução de Aterosclerose Acelerada em Camundongos: O Modelo de "Lesão por Fio"

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.

Reprodutível Arterial Desnudamento Lesão por aorta abdominal infrarrenal fixação num 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.

O modelo de coelho da aterosclerose acelerada: uma perspectiva metodológica da artéria ilíaca balão lesão

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.

Uma lesão de balão segmental controlada por pressão da artéria de rato com aplicação terapêutica periadventicional

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.

Lesão por esmagamento aórtico murino: um eficiente<em&gt; In Vivo</em&gt; Modelo de proliferação de células musculares lisas e função endotelial

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

Biologia

<meta charset="utf8"></head><body>Investigando os mecanismos moleculares subjacentes ao aneurisma da aorta abdominal murina

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 em destaque: Desenvolvimento e caracterização de um modelo de camundongo para aneurisma da 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.

Um modelo de aneurisma de aorta abdominal de camundongo por infiltração periadventícia de cloreto de cálcio e elastase

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

Lesão baseada no balão para induzir a hiperplasia Myointimal da Aorta Abdominal de Mouse

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