Abstract 357: Intra-placental gene transfer of Insulin Like Growth Factor 1 Reprograms Altered Myocardial Gene Expression In Growth Restricted Mouse Model with Cardiac Dysfunction

التفاصيل البيبلوغرافية
العنوان: Abstract 357: Intra-placental gene transfer of Insulin Like Growth Factor 1 Reprograms Altered Myocardial Gene Expression In Growth Restricted Mouse Model with Cardiac Dysfunction
المؤلفون: khaled R omar, Tarek Alsaeid, Charles Klanke, Ahmed Lababidi, Mounira Habli
المصدر: Circulation Research. 115
بيانات النشر: Ovid Technologies (Wolters Kluwer Health), 2014.
سنة النشر: 2014
مصطلحات موضوعية: Physiology, Cardiology and Cardiovascular Medicine
الوصف: Background: Intrauterine growth restriction (IUGR), defined as birth weight Method: Laparotomy was performed on pregnant C57 mice at embryonic day 18 and pups were divided into 3 groups. Control: Sham operated; IUGR: by ligation of a uterine artery branch; IUGR+IGF1: injection of Ad IGF1 after ligation. Pups were delivered and followed up with cross-sectional (2D) and Doppler transthoracic echocardiography until 36 week. Hearts were collected and RNA extracted for gene expression analysis by qPCR at 36 week. Data were analyzed using ANOVA Result: At week 36, IUGR mice showed significantly reduced EF (41 ± 6 vs 53 ± 7 vs 57 ± 9) compared to SHAM & IUGR+IGF1 (Fig A). IUGR showed significantly increased LVID;d (3.8 ± 0.3 vs 3.1± 0.49 vs 2.9 ± 0.4) as compared to SHAM & IUGR+IGF1 (Fig B). IUGR hearts demonstrated significantly increased CTGF (1.7± 0.6 vs 0.9 ± 0.3 vs 0.8 ± 0.2), and Col1A1 (2.4 ± 0.2 vs. 1.6 ± 0.4 vs 1.4 ± 0.5), as compared to SHAM & IUGR+IGF1(Fig C). No differences were detected in the other genes Conclusion: AdIGF1 gene transfer rescues IUGR induced cardiac dysfunction and reprograms myocardial gene expression of CTGF&COL1A1. These changes may represent a potential epigenetic regulation that reprograms the fetus and attenuates the risk of adult onset CVD
تدمد: 1524-4571
0009-7330
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::67e73e1d11500a71005336c5e2930348
https://doi.org/10.1161/res.115.suppl_1.357
رقم الأكسشن: edsair.doi...........67e73e1d11500a71005336c5e2930348
قاعدة البيانات: OpenAIRE