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Targeted deletion of p53 prevents cardiac rapture after myocardial infarction in mice

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Title: Targeted deletion of p53 prevents cardiac rapture after myocardial infarction in mice
Authors: Matsusaka, Hidenori Browse this author
Ide, Tomomi Browse this author
Matsushima, Shouji Browse this author
Ikeuchi, Masaki Browse this author
Kubota, Toru Browse this author
Sunagawa, Kenji Browse this author
Kinugawa, Shintaro Browse this author
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Keywords: adoptosis
extracellular matrix
Issue Date: 1-Jun-2006
Publisher: Elsevier
Journal Title: Cardiovascular research
Volume: 70
Issue: 3
Start Page: 457
End Page: 465
Publisher DOI: 10.1016/j.cardiores.2006.02.001
Abstract: Objective Apoptosis may play an important role in cardiac remodeling after myocardial infarction (MI). p53 is a well-known proapoptotic factor. However, its pathophysiological significance in these conditions remains unclear. We thus examined the effects of target deletion of the p53 gene on post-MI hearts. Methods Anterior MI was created in male heterozygous p53-deficient (p53+/−; n = 28) mice and sibling wild-type (p53+/+; n = 29) mice by ligating the left coronary artery. Results By day 7, p53+/− mice had significantly better survival rate than p53+/+ mice (89% vs. 69%, P < 0.05). Notably, p53+/− mice had a significantly lower incidence of left ventricular (LV) rupture (7% vs. 28%, P < 0.05) despite comparable infarct size (60 ± 2% vs. 59 ± 2%, P = NS), heart rate (488 ± 15 vs. 489 ± 17 bpm, P = NS), or mean arterial blood pressure (80 ± 2 vs. 78 ± 3 mm Hg, P = NS). The extent of infiltrating interstitial cells including macrophages into the post-MI hearts was not altered by the deletion of p53. Further, collagen deposition as well as the zymographic MMP-2 and -9 activities were comparable between p53+/− and p53+/+ mice with MI. However, the p53+/− mice had a significantly thicker infarct wall. The number of TUNEL-positive cells in the infarct area was significantly lower in p53+/− mice than in p53+/+ mice (423 ± 86 vs. 1330 ± 275/105 cells, P < 0.01). Conclusions p53 is involved in cardiac rupture after MI, probably via the induction of a proapoptotic pathway. The inhibition of p53 may be a potentially useful therapeutic strategy to manage post-MI patients.
Rights: Copyright © 2006 European Society of Cardiology Published by Elsevier B.V.
Type: article (author version)
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 筒井 裕之

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