2013 conference-abstract

Abstract 312: STIM1 And The Development Of Pressure-overload Induced Cardiac Hypertrophy In Rodents

Ludovic Bénard, Daniel S. Matasic, Mathilde Keck, Anne‐Marie Lompré, Roger J. Hajjar, Jean‐Sébastien Hulot

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3Institutions déclarées

3Pays d’affiliation déclarés

Rattachement africain : us, it, fr. Niveau de preuve : code pays fourni par la source.

Le résumé fourni par la source

STromal Interaction Molecule 1 (STIM1), a membrane protein of the sarcoplasmic reticulum, has recently been proposed as a positive regulator of cardiomyocyte growth by promoting Ca2+ entry through the plasma membrane and the activation of Ca2+-mediated signaling pathways. We studied the role of STIM1 in a pressure-overload induced cardiac hypertrophy model in mice. We observed that STIM1 cardiac expression is increased during left ventricular hypertrophy (LVH) induced by Transverse Aortic Constriction (TAC). We then used recombinant Associated Adenovirus 9 (AAV9) to perform cardiac-targeted gene silencing in vivo. C57Bl/6 mice were injected with saline (noAAV) or with AAV9 expressing shRNA against STIM1 (shSTIM1) at the dose of 1e+11 viral genome which resulted in 70% decrease of STIM1 cardiac expression compared to control mice. Three weeks later, TAC was performed and mice were studied three other weeks later. We found that TAC-shSTIM1 treated mice did not develop LVH compared to noAAV despite the same increase in aortic pressure. Echocardiographic and hemodynamic measurements (see table) showed that TAC-shSTIM1-treated mice had LV dilation and a decreased left ventricular contractile function in line with the absence of compensatory LVH in these mice. Immunohistochemistry demonstrated that LVH prevention was observed at the cellular level with cardiac myocytes cross-section area comparable to sham littermates however with a trend towards more interstitial fibrosis. This study reveals the essential role of STIM1 in the development of compensatory LVH in mice.

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Le contrôle bibliographique ouvert

DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.

Titre Crossref: Abstract 312: STIM1 And The Development Of Pressure-overload Induced Cardiac Hypertrophy In Rodents
Date Crossref: 01/08/2013
Éditeur: Ovid Technologies (Wolters Kluwer Health)
Type: journal-article

Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.

Où se fait cette recherche

Icahn School of Medicine at Mount Sinai pays non établi dans la notice
Université ou école supérieure
Danieli (Italy) pays non établi dans la notice
Entreprise
Inserm pays non établi dans la notice
Organisme public
Icahn Sch of Medicine at Mount Sinaï pays non établi dans la notice
Institution
Daniel S Matasic pays non établi dans la notice
Institution
Mathilde Keck pays non établi dans la notice
Institution
Roger J Hajjar pays non établi dans la notice
Institution

Icahn School of Medicine at Mount Sinai, Danieli (Italy) et Inserm, avec 4 autres affiliations.

Une affiliation ne permet pas de déduire la nationalité d’un auteur.

Les sujets associés

Cardiac Fibrosis and RemodelingCardiovascular Effects of Exercise

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