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Effect of lipopolysaccharide on the expression of VWF and ADAMTS13 in rat pulmonary microvascular endothelial cells and the intervention of vitamin D |
Xu Jun, Yang Jia-lai, Chen Jian, Luo Qing-li, Meng Ling-yi, Yu Feng, Zhang Hong |
Department of Emergency, the First People’s Hospital of Hefei, the Third Affiliated Hospital of Anhui Medical University, Hefei 230001, China |
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Abstract Objective To observe the effects of lipopolysaccharide(LPS)on cultured rat pul⁃ monary microvascular endothelial cells(PMVEC)von Willebrand factor(VWF), A disintegrin- likeandmetalloproteinase with thrombospond in type-1 domain 13(ADAMTS13)expression, and the inter⁃ vention effect of vitamin D(Vit D). Methods Primary cultured rat PMVEC were randomly assigned to 6 groups: NC group, LPS group(given 100 μg /mL LPS)and calcitriol(Cal)group(given 100 nmol/L Cal), LPS+Cal 1, 2, 3 groups(treated with 100 μg /mL LPS and 5 nmol/l, 20 nmol/L, 100 nmol/L Cal) were used to detect the expression of VWF and ADAMTS13 mRNA and protein in cell lysates. Results VWF, ADAMTS13 mRNA and protein expression showed no significant changes in LPS group and Cal group, VWF mRNA and protein expression levels in LPS group and LPS + Cal groups were significantly higher than those in NC group; VWF mRNA and protein expression levels in LPS + Cal groups of were significantly lower than those in LPS group; ADAMTS13 mRNA and protein expression levels in LPS group and LPS + Cal groups were significantly lower than those in NC group; ADAMTS13 mRNA and protein expression levels in LPS+Cal 3 group were significantly higher than those in the LPS group. Conclusion Vit D in physiological condition does not change the expression of VWF and ADAMTS13 in PMVECs, while after being stimulated by LPS Vit D can prevent the increase of VWF expression and the reduction of ADAMTS13 caused by LPS. In the pathogenesis of sepsis or ALI, Vit D may play a role in the disease outcome by affecting the expression of VWF and ADAMTS13 in PMVEC.
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Corresponding Authors:
Zhang Hong, E-mail: tianlin200401@126.com
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