Stim1- and Orai1-mediated store-operated calcium entry is critical for angiotensin II-induced vascular smooth muscle cell proliferation.
Cardiovasc Res
; 93(2): 360-70, 2012 Feb 01.
Article
en En
| MEDLINE
| ID: mdl-22108917
AIM: Despite the fact that angiotensin (Ang) II is a critical regulator of the proliferation and migration of vascular smooth muscle cells (VSMCs), the effect of Ang II on VSMC proliferation has remained unclear. In this study, we determined whether Stim1- and Orai1-mediated store-operated calcium (Ca(2+)) entry (SOCE) plays a critical role in Ang II-induced VSMC proliferation and Ang II-accelerated neointimal growth after balloon injury of rat carotid arteries. METHODS AND RESULTS: Knockdown of Stim1 and Orai1, putative calcium sensors/modulators, suppressed Ang II-mediated Ca(2+) entry and cell proliferation in synthetic VSMCs. Stim1 and Orai1 short interfering RNAs (siRNAs) decreased neointimal growth induced by Ang II in balloon-injured rat carotid arteries. Ang II signiï¬cantly increased the expression of Stim1 and Orai1 in neointima. In addition, our results showed that receptor subtype-1 (AT1) significantly contributed to Ang II-induced Ca(2+) entry and proliferation of synthetic VSMCs. However, we found that transient receptor potential canonical 1 (Trpc1) had no effect on Ang II-induced SOCE or cell proliferation of synthetic VSMCs. CONCLUSIONS: We show for the first time that Stim1- and Orai1-mediated SOCE may be critical for Ang II-induced VSMC proliferation. This provides important information with respect to targeting cardiovascular diseases under the enhanced renin-Ang system.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Angiotensina II
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Glicoproteínas de Membrana
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Canales de Calcio
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Calcio
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Miocitos del Músculo Liso
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Proliferación Celular
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Músculo Liso Vascular
Límite:
Animals
Idioma:
En
Revista:
Cardiovasc Res
Año:
2012
Tipo del documento:
Article
País de afiliación:
China
Pais de publicación:
Reino Unido