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Resolvin D1 blocks ROS‐mediated inhibitory crosstalk between SHP2 and PP2A and suppresses endothelial‐monocyte interactions
Abstract   Open access   Peer reviewed

Resolvin D1 blocks ROS‐mediated inhibitory crosstalk between SHP2 and PP2A and suppresses endothelial‐monocyte interactions

Nikhlesh Singh, Rima N. Chattopadhyay, Arul M. Mani and Gadiparthi N. Rao
The FASEB journal, Vol.32(S1), pp.574.3-574.3
04/2018
DOI: 10.1096/fasebj.2018.32.1_supplement.574.3
url
https://doi.org/10.1096/fasebj.2018.32.1_supplement.574.3View
Published (Version of record) Open Access

Abstract

In recent years, various studies have demonstrated a role for endogenously derived specialized lipid mediators such as resolvins in the resolution of inflammation. In exploring the signaling mechanisms, in the present study, we show that RvD1 reduces LPS‐induced endothelial cell (EC)‐monocyte interactions via blocking ROS‐mediated PP2A inactivation, NFκB activation and ICAM1 and VCAM1 expression. In addition, we found that ROS‐mediated SHP2 inhibition leads to tyrosine phosphorylation and inactivation of PP2A by LPS, which in turn, accounts for increased NFκB activation and ICAM1 and VCAM1 expression facilitating EC‐monocyte interactions and all these LPS‐mediated responses were reversed by RvD1. Furthermore, the suppression of NFκB activation, ICAM1 and VCAM1 expression and EC and monocyte interactions by RvD1 involved its receptors ALX/FPR2 and GPR32 as inhibition or neutralization of these receptors negated its effects. Together, these observations show that RvD1 via protecting SHP2 from ROS‐mediated inactivation blocks PP2A inactivation and thereby shuts of NFκB activation, ICAM1 and VCAM1 expression and EC‐monocyte interactions, which could be one of the several possible mechanisms underlying its anti‐inflammatory functions. This is from the Experimental Biology 2018 Meeting. There is no full text article associated with this published in The FASEB Journal.

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