IL-10 Accelerates Re-Endothelialization and Inhibits Post-Injury Intimal Hyperplasia following Carotid Artery Denudation

PloS One
Suresh K VermaRaj Kishore

Abstract

The role of inflammation on atherosclerosis and restenosis is well established. Restenosis is thought to be a complex response to injury, which includes early thrombus formation, acute inflammation and neo-intimal growth. Inflammatory cells are likely contributors in the host response to vascular injury, via cytokines and chemokines secretion, including TNF-alpha (TNF). We have previously shown that IL-10 inhibits TNF and other inflammatory mediators produced in response to cardiovascular injuries. The specific effect of IL-10 on endothelial cell (ECs) biology is not well elucidated. Here we report that in a mouse model of carotid denudation, IL-10 knock-out mice (IL-10KO) displayed significantly delayed Re-endothelialization and enhanced neo-intimal growth compared to their WT counterparts. Exogenous recombinant IL-10 treatment dramatically blunted the neo-intimal thickening while significantly accelerating the recovery of the injured endothelium in WT mice. In vitro, IL-10 inhibited negative effects of TNF on ECs proliferation, ECs cell cycle, ECs-monocyte adhesion and ECs apoptosis. Furthermore, IL-10 treatment attenuated TNF-induced smooth muscle cells proliferation. Our data suggest that IL-10 differentially regulate endot...Continue Reading

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Citations

Jul 25, 2019·Cell Adhesion & Migration·Sona CejkovaIvana Kralova Lesna
Jun 26, 2020·Current Gerontology and Geriatrics Research·Eleni SertedakiFragiska Sigala
Aug 8, 2017·The Journal of Clinical Investigation·Miguel QuirosAsma Nusrat
Sep 2, 2017·Cardiovascular Research·Jyoti Patel
Oct 20, 2020·Advanced Healthcare Materials·Gabriel J M MirhaidariChristopher K Breuer
Jun 13, 2021·Molecular Biology Reports·Rebecca KuanFinosh G Thankam

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Methods Mentioned

BETA
transfection

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NIH ImageJ
GraphPad prism

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