Increasing extracellular Ca2 +sensitizes TNF-alpha-induced vascular cell adhesion molecule-1 (VCAM-1) via a TRPC1/ERK1/2/NFκB-dependent pathway in human vascular endothelial cells

Songtao Li, Hua Ning, Yaxin Ye, Wei Wei, Rui Guo, Qing Song, Lei Liu, Yunyun Liu, Lixin Na, Yuchun Niu, Xia Chu, Rennan Feng, Naima Moustaid-Moussa, Ying Li, Changhao Sun

Research output: Contribution to journalArticle

Abstract

© 2017 Elsevier B.V. Increasing circulating Ca 2 + levels within the normal range has been reported to positively correlate with the incidence of fatal cardiovascular diseases (CVDs). However, limited studies have been able to delineate the potential mechanism(s) linking circulating Ca 2 + to CVD. In this study, we exposed primary human umbilical vein endothelial cells (HUVECs) and human umbilical vein cell line (EA.hy926) to different extracellular Ca 2 + to mimic the physiological state. Our data revealed that increasing extracellular Ca 2 + significantly enhanced susceptibility to tumor necrosis factor (TNF)-alpha-stimulated vascular cell adhesion molecule (VCAM)-1 expression and monocytes adhesion. Knocking-down VCAM-1 by siRNA abolished calcium-induced monocytes adhesion on HUVECs. Follow up mechanistic investigations identified that extracellular Ca 2 + -increased calcium influx contributed to the activation of VCAM-1. This was mediated via upregulation of transient receptor pot
Original languageEnglish
Pages (from-to)1566-1577
JournalBiochimica et Biophysica Acta - Molecular Cell Research
StatePublished - Oct 1 2017

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