Abstract
Objectives: Hyperproliferation of vascular smooth muscle cells (VSMC) is a major risk factor for cardiovascular diseases. Proper mitochondrial fission and fusion is involved with VSMC function. However, the role and mechanism of mitochondrial morphological changes in VSMC proliferation are not well understood. Methods: Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHRs) were used in this study. The expression of calcium sensing receptor (CaSR) and proteins of mitochondrial dynamics was determined by werstern blot. Primary VSMC stimulated with angiotensin II (Ang II) was used to mimic hypertension in vitro. Results: We found that CaSR was increased in the aortas from SHRs compared with age-matched WKY rats. There was also an increase in mitochondrial fission and VSMC proliferation, which was attenuated by Calhex231. In primary rat VMSC, Ang II stimulation induced cytosolic [Ca2+]i increase, mitochondrial shortening and proliferation, all of which could be attenuated by pretreatment with mitochondrial division inhibitor-1 and Calhex231. Conclusion: Our data indicate that CaSR-mediated mitochondrial fission could be a therapeutic target for hyperproliferative disorders.
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