Open Access
Fluid shear stress modulates endothelial inflammation by targeting LIMS2
Author(s) -
Junyao Wang,
Shiyanjin Zhang
Publication year - 2020
Publication title -
experimental biology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.012
H-Index - 146
eISSN - 1535-3702
pISSN - 1535-3699
DOI - 10.1177/1535370220943837
Subject(s) - mechanosensitive channels , inflammation , microbiology and biotechnology , in vivo , endothelial dysfunction , biology , gene , pathophysiology , endothelium , shear stress , immunology , genetics , endocrinology , receptor , ion channel , materials science , composite material
Mechanosensitive genes regulate multiple cardiovascular pathophysiological processes and disorders; however, the role of flow-sensitive genes in atherosclerosis is still unknown. In this study, we identify LIM Zinc Finger Domain Containing 2 (LIMS2) that acts as a mechanosensitive gene downregulated by disturbed flow (d-flow) both in human endothelial cells (ECs) in vitro and in mice in vivo . Mechanistically, d-flow suppresses LIMS2 expression, which leads to endothelial inflammation by upregulating typical inflammatory factors, VCAM-1, and ICAM-1 in human ECs. The findings indicate that LIMS2, the new flow-sensitive gene, may help us to find a new insight to explain how d-flow caused endothelial inflammation and provide a new therapeutic approach for atherosclerosis in the future.