Study on the mechanism of miR-155 regulating CaSR expression and affecting the growth of vascular smooth muscle cells
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Department of Critical Care Medicine, Jinzhou Medical University, Jinzhou, Liaoning 121001, China)

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R54

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    Abstract:

    Aim miR-155 can inhibit the formation of atherosclerotic plaques by interfering with the biological activity of vascular smooth muscle cells, but the specific mechanism is not very clear. The purpose of this study was to observe the effects of miR-155 on calcium sensing receptor(CaSR) expression in vascular smooth muscle cells, and to explore the role of CaSR in miR-155 in regulating the biological activity of vascular smooth muscle cells. Methods Vascular smooth muscle cells were cultured, and miR-155 mimic and Ad-CaSR were transfected into vascular smooth muscle cells. Western blot was used to detect the expression of related genes. MTT was used to determine the growth of vascular smooth muscle cells. Flow cytometry was used to detect the apoptosis of vascular smooth muscle cells. Transwell was used to detect the migration of vascular smooth muscle cell. Results The expression level of CaSR in miR-155 mimic group was significantly inhibited, the apoptosis of vascular smooth muscle cells was significantly reduced, and the proliferation and migration capabilities of vascular smooth muscle cells were significantly enhanced. Apoptosis of the cells was significantly increased, while the proliferation and migration capacity of vascular smooth muscle cells was significantly reduced. Conclusion miR-155 can regulate the growth of vascular smooth muscle cells, but this effect may be achieved by affecting the activity of CaSR in vascular smooth muscle cells.

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JIN Zihan, ZHANG Jianing, FENG Lu, ZHANG Fengxiang. Study on the mechanism of miR-155 regulating CaSR expression and affecting the growth of vascular smooth muscle cells[J]. Editorial Office of Chinese Journal of Arteriosclerosis,2021,29(3):201-205.

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History
  • Received:August 21,2020
  • Revised:December 23,2020
  • Online: March 02,2021
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