IP3 and calcium signaling involved in the reorganization of the actin cytoskeleton and cell rounding induced by cigarette smoke extract in human endothelial cells

Environmental Toxicology
Bo-Hong LinTsu-Shing Wang

Abstract

Smoking increases the risk of cardiovascular disorders and leads to damage caused by inflammation and oxidative stress. The actin cytoskeleton is a key player in the response to inflammatory stimuli and is an early target of cellular oxidative stress. The purpose of this study was to investigate the changes in actin cytoskeleton dynamics in human endothelial EA.hy926 cells exposed to cigarette smoke extract (CSE). Immunostaining revealed that CSE exposure resulted in modification of the actin cytoskeleton and led to cell rounding in a dose- and time-dependent manner. In addition, the intracellular calcium concentration was increased by treatment with CSE. Pretreatment with antioxidants (lipoic acid, glutathione, N-acetyl cysteine, aminoguanidine, α-tocopherol, and vitamin C) significantly attenuated the CSE-induced actin cytoskeleton reorganization and cell rounding. Calcium ion chelators (EGTA, BAPTA-AM AM) and a potent store-operated calcium channel inhibitor (MRS 1845) also reduced CSE-induced intracellular calcium changes and attenuated actin cytoskeleton reorganization and cell morphology change. Moreover, the CSE-induced intracellular calcium increase was suppressed by pretreatment with the inositol trisphosphate receptor...Continue Reading

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Citations

Aug 22, 2018·Expert Opinion on Investigational Drugs·Yu-Long LanBo Zhang
Jan 17, 2019·Immunologic Research·Jarek WosikMalgorzata Kloc
Apr 4, 2019·American Journal of Respiratory Cell and Molecular Biology·Aurelie PetitArnaud Bourdin
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Jun 2, 2021·Journal of Cellular and Molecular Medicine·Qiang ZhangYuanyi Yue
Aug 25, 2020·ACS Chemical Neuroscience·Adithya MohandassBaskaran Thyagarajan

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