Piezo1 in endothelial cells is involved in vitamin D-induced vascular calcification

The relationship between the Piezo1 channel of vascular endothelial cells and vascular calcification is unknown. In this study, after subcutaneous injection of vitamin D for 10 consecutive days, the mice showed an increase in serum calcium, aortic calcium content, vascular tension and pulse wave vel...

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Veröffentlicht in:Biochemical and biophysical research communications 2023-01, Vol.638, p.140-146
Hauptverfasser: Liu, Zhihui, Tong, Tong, Sun, Jinglei, Wu, Wenting, Zhang, Jiali, Cui, Ziyang, Han, Mei
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Sprache:eng
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Zusammenfassung:The relationship between the Piezo1 channel of vascular endothelial cells and vascular calcification is unknown. In this study, after subcutaneous injection of vitamin D for 10 consecutive days, the mice showed an increase in serum calcium, aortic calcium content, vascular tension and pulse wave velocity. Piezo1channel antagonist, GsMTx4 alleviated arteriosclerosis and decreased the aortic calcium content, while Piezo1 agonist Yoda1 produced opposite effect. In addition, activation of Piezo1 by Yoda1 impaired the function of human umbilical vein endothelial cells (HUVECs), as evidenced by further decreased production of NO, reduction in expression levels of eNOS, MMP-2, PCNA and VEGFA. When co-culture of HUVECs and vascular smooth muscle cells (VSMCs), activation of Piezo1 in HUVECs enhanced expression levels of calcification-related SOX9 and Runx2 genes, increased ALP activity and calcium deposition in VSMCs. We concluded that Piezo1 in endothelial cells is involved in the pathogenesis of vascular calcification. This study provides a new experimental basis for the prevention and treatment of vascular calcification. •This study first demonstrated that Piezo1 channel antagonist alleviated vitamin D-induced vascular calcification in mice.•Activation of Piezo1 in endothelial cells promoted osteogenic transformation of vascular smooth muscle cells.•This study provides a new experimental basis for the prevention and treatment of vascular calcification.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2022.11.060