Stim1- and Orai1-mediated store-operated calcium entry is critical for angiotensin II-induced vascular smooth muscle cell proliferation. 2012

Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
Department of Cardiology, Kunming General Hospital of Chengdu Military Area, Yunnan 650032, China.

OBJECTIVE 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. 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 significantly 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.

UI MeSH Term Description Entries
D008297 Male Males
D008562 Membrane Glycoproteins Glycoproteins found on the membrane or surface of cells. Cell Surface Glycoproteins,Surface Glycoproteins,Cell Surface Glycoprotein,Membrane Glycoprotein,Surface Glycoprotein,Glycoprotein, Cell Surface,Glycoprotein, Membrane,Glycoprotein, Surface,Glycoproteins, Cell Surface,Glycoproteins, Membrane,Glycoproteins, Surface,Surface Glycoprotein, Cell,Surface Glycoproteins, Cell
D009131 Muscle, Smooth, Vascular The nonstriated involuntary muscle tissue of blood vessels. Vascular Smooth Muscle,Muscle, Vascular Smooth,Muscles, Vascular Smooth,Smooth Muscle, Vascular,Smooth Muscles, Vascular,Vascular Smooth Muscles
D002118 Calcium A basic element found in nearly all tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes. Coagulation Factor IV,Factor IV,Blood Coagulation Factor IV,Calcium-40,Calcium 40,Factor IV, Coagulation
D000071737 Stromal Interaction Molecule 1 A stromal interaction molecule that functions in the regulation of calcium influx following depletion of intracellular calcium in the ENDOPLASMIC RETICULUM. It translocates to the plasma membrane upon calcium depletion where it activates the CALCIUM RELEASE ACTIVATED CALCIUM CHANNEL ORAI1. STIM1 Protein
D000071740 ORAI1 Protein The pore-forming subunit of calcium release activated calcium channels. It is activated by STROMAL INTERACTION MOLECULE 1 upon intracellular calcium depletion. Calcium Release-Activated Calcium Channel Protein 1,ORAI Calcium Release-Activated Calcium Modulator 1,Calcium Release Activated Calcium Channel Protein 1,ORAI Calcium Release Activated Calcium Modulator 1
D000804 Angiotensin II An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS. Angiotensin II, Ile(5)-,Angiotensin II, Val(5)-,5-L-Isoleucine Angiotensin II,ANG-(1-8)Octapeptide,Angiotensin II, Isoleucine(5)-,Angiotensin II, Valine(5)-,Angiotensin-(1-8) Octapeptide,Isoleucine(5)-Angiotensin,Isoleucyl(5)-Angiotensin II,Valyl(5)-Angiotensin II,5 L Isoleucine Angiotensin II,Angiotensin II, 5-L-Isoleucine
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D015220 Calcium Channels Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue. Ion Channels, Calcium,Receptors, Calcium Channel Blocker,Voltage-Dependent Calcium Channel,Calcium Channel,Calcium Channel Antagonist Receptor,Calcium Channel Antagonist Receptors,Calcium Channel Blocker Receptor,Calcium Channel Blocker Receptors,Ion Channel, Calcium,Receptors, Calcium Channel Antagonist,VDCC,Voltage-Dependent Calcium Channels,Calcium Channel, Voltage-Dependent,Calcium Channels, Voltage-Dependent,Calcium Ion Channel,Calcium Ion Channels,Channel, Voltage-Dependent Calcium,Channels, Voltage-Dependent Calcium,Voltage Dependent Calcium Channel,Voltage Dependent Calcium Channels
D017208 Rats, Wistar A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain. Wistar Rat,Rat, Wistar,Wistar Rats

Related Publications

Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
May 2011, Journal of applied physiology (Bethesda, Md. : 1985),
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
November 2008, Circulation research,
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
January 2017, Cell death discovery,
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
November 2013, Cardiovascular research,
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
March 2008, British journal of pharmacology,
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
August 2009, FASEB journal : official publication of the Federation of American Societies for Experimental Biology,
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
February 2009, The Journal of biological chemistry,
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
January 2013, Current topics in membranes,
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
December 2018, Cell calcium,
Rui-wei Guo, and Li-xia Yang, and Mao-quan Li, and Xing-hua Pan, and Bei Liu, and Yong-li Deng
March 2014, The Journal of biological chemistry,
Copied contents to your clipboard!