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H9N2 swine influenza virus infection-induced damage is mediated by TRPM2 channels in mouse pulmonary microvascular endothelial cells.

Abstract：

:Oxidative stress is implicated in the pathogenesis of influenza virus infection. Increasing evidences show that transient receptor potential melastatin 2 (TRPM2), a Ca2+-permeable non-selective cation channel, plays an important role in the pathomechanism of reactive oxygen species (ROS)-coupled diseases. The present study investigated the role of TRPM2 in pulmonary microvascular endothelial cells (PMVECs) during H9N2 influenza virus infection. We knocked down TRPM2 in PMVECs using TRPM2 shRNA lentiviral particles. Subsequently, we utilized enzyme-linked immunosorbent assay and flow cytometry to compare ROS levels, DNA damage, mitochondrial integrity, apoptosis, and inflammatory factors between control and TRPM2-knockdown PMVECs following H9N2 influenza virus infection. Inhibition of TRPM2 channels reduced H9N2 virus-induced intracellular ROS production, decreased DNA damage, and inhibited H9N2-induced cellular apoptosis. This study shows that the inhibition of TRPM2 channels may protect PMVECs from the damage caused by H9N2 virus infection. Our results highlight the importance of TRPM2 in modulating ROS production, apoptosis, mitochondrial dysfunction, cytokine expression, and DNA damage in H9N2 virus-infected PMVECs, and suggest that TRPM2 may be a potential antiviral target.

journal_name

Microb Pathog

journal_title

Microbial pathogenesis

authors

Wang S,Liang T,Luo Q,Li P,Zhang R,Xu M,Su J,Xu T,Wu Q

doi

10.1016/j.micpath.2020.104408

subject

Has Abstract

pub_date

2020-11-01 00:00:00

pages

104408

eissn

0882-4010

issn

1096-1208

pii

S0882-4010(20)30774-9

journal_volume

148

pub_type

杂志文章

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