| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10765578 | Biochemical and Biophysical Research Communications | 2009 | 5 Pages |
Abstract
Store-operated Ca2+ entry (SOCE) through transient receptor potential (TRP) channels is important in the development of cardiac hypertrophy. Recently, stromal interaction molecule 1 (STIM1) was identified as a key regulator of SOCE. In this study, we examined whether STIM1 is involved in the development of cardiomyocyte hypertrophy. RT-PCR showed that cultured rat cardiomyocytes constitutively expressed STIM1. Endothelin-1 (ET-1) treatment for 48Â h enhanced TRPC1 expression, SOCE, and nuclear factor of activated T cells activation without upregulating STIM1. However, the knockdown of STIM1 suppressed these effects, thereby preventing a hypertrophic response. These results suggest that STIM1 plays an essential role in the development of cardiomyocyte hypertrophy.
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Authors
Takayoshi Ohba, Hiroyuki Watanabe, Manabu Murakami, Takako Sato, Kyoichi Ono, Hiroshi Ito,