Functional role of stromal interaction molecule 1 (STIM1) in vascular smooth muscle cells

Journal Article · Fri Oct 05 04:00:00 EDT 2007 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/j.bbrc.2007.07.096· OSTI ID:21032911

Takahashi, Yoichiro; Watanabe, Hiroyuki ^[1]; Murakami, Manabu; Ono, Kyoichi ^[2]; Munehisa, Yoshiko; Koyama, Takashi; Nobori, Kiyoshi ^[1]; Iijima, Toshihiko ^[2]; Ito, Hiroshi ^[1]

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1. Second Department of Internal Medicine, Akita University School of Medicine, 1-1-1 Hondo, Akita 010-8543 (Japan)
2. Department of Pharmacology, Akita University School of Medicine, Akita (Japan)

We investigated the functional role of STIM1, a Ca{sup 2+} sensor in the endoplasmic reticulum (ER) that regulates store-operated Ca{sup 2+} entry (SOCE), in vascular smooth muscle cells (VSMCs). STIM1 was mainly localized at the ER and plasma membrane. The knockdown of STIM1 expression by small interfering (si) RNA drastically decreased SOCE. In contrast, an EF-hand mutant of STIM1, STIM1{sup E87A}, produced a marked increase in SOCE, which was abolished by co-transfection with siRNA to transient receptor potential canonical 1 (TRPC1). In addition, transfection with siRNA against STIM1 suppressed phosphorylation of cAMP-responsive element binding protein (CREB) and cell growth. These results suggest that STIM1 is an essential component of SOCE and that it is involved in VSMC proliferation.

• OSTI ID: 21032911
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 4 Vol. 361; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
AMP
CALCIUM IONS
ENDOPLASMIC RETICULUM
MEMBRANES
MUSCLES
MUTANTS
PHOSPHORYLATION
RECEPTORS
RNA