gp130 Plays a Critical Role in Pressure Overload-induced Cardiac Hypertrophy

Hiroki Uozumi, Yukio Hiroi, Yunzeng Zou, Eiki Takimoto, Haruhiro Toko, Pei Niu, Masaki Shimoyama, Yoshio Yazaki, Ryozo Nagai, Issei Komuro

Research output: Contribution to journalArticlepeer-review

67 Scopus citations


gp130, a common receptor for the interleukin 6 family, plays pivotal roles in growth and survival of cardiac myocytes. In the present study, we examined the role of gp130 in pressure overload-induced cardiac hypertrophy using transgenic (TG) mice, which express a dominant negative mutant of gp130 in the heart under the control of α myosin heavy chain promoter. TG mice were apparently healthy and fertile. There were no differences in body weight and heart weight between TG mice and littermate wild type (WT) mice. Pressure overload-induced increases in the heart weight/body weight ratio, ventricular wall thickness, and cross-sectional areas of cardiac myocytes were significantly smaller in TG mice than in WT mice. Northern blot analysis revealed that pressure overload-induced up-regulation of brain natriuretic factor gene and down-regulation of sarcoplasmic reticulum Ca2+ ATPase 2 gene were attenuated in TG mice. Pressure overload activated ERKs and STAT3 in the heart of WT mice, whereas pressure overload-induced activation of STAT3, but not of ERKs, was suppressed in TG mice. These results suggest that gp130 plays a critical role in pressure overload-induced cardiac hypertrophy possibly through the STAT3 pathway.

Original languageEnglish (US)
Pages (from-to)23115-23119
Number of pages5
JournalJournal of Biological Chemistry
Issue number25
StatePublished - Jun 22 2001
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry


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