Literature DB >> 11869860

The antioxidant N-2-mercaptopropionyl glycine attenuates left ventricular hypertrophy in in vivo murine pressure-overload model.

Moto-o Date1, Takashi Morita, Nobushige Yamashita, Kazuhiko Nishida, Osamu Yamaguchi, Yoshiharu Higuchi, Shinichi Hirotani, Yasushi Matsumura, Masatsugu Hori, Michihiko Tada, Kinya Otsu.   

Abstract

OBJECTIVES: In order to identify the role of reactive oxygen species (ROS) in cardiac hypertrophy, we examined the effect of N-2-mercaptopropionyl glycine (MPG) on cardiac hypertrophy.
BACKGROUND: Recent in vitro studies have suggested that ROS play an important role as a second messenger in cardiac hypertrophy. It was therefore thought to be of particular value to examine the relevance of studies using in vitro models for cardiac hypertrophy in an in vivo setting.
METHODS: The transverse thoracic aorta in mice was constricted, and MPG (100 mg/kg) was infused intraperitoneally twice daily. The animals were assessed seven days after the operation for hemodynamic functions, oxidative stress and antioxidative enzyme activities.
RESULTS: Banding of the transverse aorta in mice resulted in an increase in the ratio of heart weight to tibia length and the appearance of an endogenous atrial natriuretic factor messenger ribonucleic acid (mRNA) seven days postoperatively. Administration of MPG significantly attenuated the hypertrophic responses induced by pressure overload. Cardiac hypertrophy was accompanied by increases in heme oxygenase-1 mRNA expression and lipid peroxidation, which was eliminated by the treatment with MPG. Pressure overload led to increases in antioxidant enzyme activities, such as superoxide dismutase and glutathione peroxidase, but not catalase, activity.
CONCLUSIONS: Our results indicated that oxidative stress was increased in our model and that it plays an important role in the development of cardiac hypertrophy.

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Year:  2002        PMID: 11869860     DOI: 10.1016/s0735-1097(01)01826-5

Source DB:  PubMed          Journal:  J Am Coll Cardiol        ISSN: 0735-1097            Impact factor:   24.094


  48 in total

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2.  Mitochondrial reactive oxygen species production and respiratory complex activity in rats with pressure overload-induced heart failure.

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4.  Cytosolic H2O2 mediates hypertrophy, apoptosis, and decreased SERCA activity in mice with chronic hemodynamic overload.

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6.  p38alpha mitogen-activated protein kinase plays a critical role in cardiomyocyte survival but not in cardiac hypertrophic growth in response to pressure overload.

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7.  Inhibition of endogenous thioredoxin in the heart increases oxidative stress and cardiac hypertrophy.

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Review 8.  Redox signaling in cardiovascular health and disease.

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10.  Targeted deletion of apoptosis signal-regulating kinase 1 attenuates left ventricular remodeling.

Authors:  Osamu Yamaguchi; Yoshiharu Higuchi; Shinichi Hirotani; Kazunori Kashiwase; Hiroyuki Nakayama; Shungo Hikoso; Toshihiro Takeda; Tetsuya Watanabe; Michio Asahi; Masayuki Taniike; Yasushi Matsumura; Ikuko Tsujimoto; Kenichi Hongo; Yoichiro Kusakari; Satoshi Kurihara; Kazuhiko Nishida; Hidenori Ichijo; Masatsugu Hori; Kinya Otsu
Journal:  Proc Natl Acad Sci U S A       Date:  2003-12-09       Impact factor: 11.205

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