NDLI: Targeted deletion of apoptosis signal-regulating kinase 1 attenuates left ventricular remodeling

Content Provider	PubMed Central
Author	Yamaguchi, Osamu Higuchi, Yoshiharu Shinichi, Hirotani Kashiwase, Kazunori Nakayama, Hiroyuki Hikoso, Shungo Takeda, Toshihiro Watanabe, Tetsuya Asahi, Michio Taniike, Masayuki Matsumura, Yasushi Tsujimoto, Ikuko Hongo, Kenichi Kusakari, Yoichiro Kurihara, Satoshi Nishida, Kazuhiko Ichijo, Hidenori Hori, Masatsugu Otsu, Kinya
Copyright Year	2003
Abstract	Left ventricular remodeling that occurs after myocardial infarction (MI) and pressure overload is generally accepted as a determinant of the clinical course of heart failure. The molecular mechanism of this process, however, remains to be elucidated. Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase that plays an important role in stress-induced apoptosis. We used ASK1 knockout mice (ASK-/-) to test the hypothesis that ASK1 is involved in development of left ventricular remodeling. ASK-/- hearts showed no morphological or histological defects. Echocardiography and cardiac catheterization revealed normal global structure and function. Left ventricular structural and functional remodeling were determined 4 weeks after coronary artery ligation or thoracic transverse aortic constriction (TAC). ASK-/- had significantly smaller increases in left ventricular end-diastolic and end-systolic ventricular dimensions and smaller decreases in fractional shortening in both experimental models compared with WT mice. The number of terminal deoxynucleotidyl transferase biotin-dUDP nick end-labeling-positive myocytes after MI or TAC was decreased in ASK-/- compared with that in WT mice. Overexpression of a constitutively active mutant of ASK1 induced apoptosis in isolated rat neonatal cardiomyocytes, whereas neonatal ASK-/- cardiomyocytes were resistant to H2O2-induced apoptosis. An in vitro kinase assay showed increased ASK1 activity in heart after MI or TAC in WT mice. Thus, ASK1 plays an important role in regulating left ventricular remodeling by promoting apoptosis.
Related Links	http://dx.doi.org/10.1073/pnas.2136717100
Ending Page	15888
Page Count	6
Starting Page	15883
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	26
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-12-23
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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