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-β1-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 α-smooth muscle actin (α-SMA) and fibronectin (FN). The transforming growth factor-β1 (TGF-β1) reduced CD31, and increased α-SMA and FN protein expression levels. Vitamin D presence led to higher protein expression of CD31, and lower protein expressions of α-SMA and FN compared to the control in the TGF-β1-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.
Highlights
Acute cardiomyopathy patients are commonly found to have low vitamin D [1], which has been associated with increased mortality in critically ill patients [2]
To correctly determine the impact of mechanical stress on human cardiac microvascular endothelial cells (HCMECs), the HCMECs were mechanically stretched at 15% elongation with a 1 Hz frequency for 6 h
The immunofluorescence assay showed that 6h stretching increased α-smooth muscle actin (α-SMA) and α-tubulin (Figure 1C–F)
Summary
Acute cardiomyopathy patients are commonly found to have low vitamin D [1], which has been associated with increased mortality in critically ill patients [2]. The administration of active vitamin D has been reported to confer cardiovascular protection and increased survival in clinical [3] and experimental researches [4,5]. Paricalcitol (25-dihydroxyvitamin D2), a vitamin D receptor (VDR) activator, is reported to improve cardiovascular health or survival in patients with advanced kidney disease who tend to have low vitamin D [6,7]. Deficiency in 25-hydroxyvitamin D (1,25(OH)2D, or vitamin D) has been associated with cardiovascular disease (CVD) risk factors, such as age, high blood pressure, obesity and diabetes [8]. The association of vitamin D with CVD risk factors have been attributed to hypertension, congestive heart failure, myocardial infarction and stroke [9]. The mechanism for CVD involving vitamin D is not clear
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