Vitamin D Attenuates Loss of Endothelial Biomarker Expression in Cardio-Endothelial Cells.

ABSTRACT: Vitamin D is associated with cardiovascular health through activating the vitamin D receptor that targets genes related to cardiovascular disease (CVD). The human cardiac microvascular endothelial cells (HCMECs) were used to develop mechanically and TGF-?1-induced fibrosis models, and the rat was used as the isoproterenol (ISO)-induced fibrosis model. The rats were injected with ISO for the first five days, followed by vitamin D injection for the consecutive three weeks before being sacrificed on the fourth week. Results showed that mechanical stretching reduced endothelial cell marker CD31 and VE-cadherin protein expressions, as well as increased ?-smooth muscle actin (?-SMA) and fibronectin (FN). The transforming growth factor-?1 (TGF-?1) reduced CD31, and increased ?-SMA and FN protein expression levels. Vitamin D presence led to higher protein expression of CD31, and lower protein expressions of ?-SMA and FN compared to the control in the TGF-?1-induced fibrosis model. Additionally, protein expression of VE-cadherin was increased and fibroblast-specific protein-1 (FSP1) was decreased after vitamin D treatment in the ISO-induced fibrosis rat. In conclusion, vitamin D slightly inhibited fibrosis development in cell and animal models. Based on this study, the beneficial effect of vitamin D may be insignificant; however, further investigation of vitamin D's effect in the long-term is required in the future.

SUBMITTER: Lai CC 

PROVIDER: S-EPMC7139430 | biostudies-literature | 2020 Mar

REPOSITORIES: biostudies-literature