Chlamydia pneumoniae Infection Induces Vascular Smooth Muscle Cell Migration and Atherosclerosis Through Mitochondrial Reactive Oxygen Species-Mediated JunB-Fra-1 Activation

• DOI: 10.3389/fcell.2022.879023
• Publication Date: 2022-04-12T08:13:21Z
• Authors: Xi Zhao; Guolin Miao; Lijun Zhang; Yuke Zhang; Huanhuan Zhao; Zhelong Xu; Beibei Wang; Lijun Zhang
• Keywords: JUNB

Infection is closely related to atherosclerosis, which a major pathological basis for cardiovascular diseases. Vascular smooth muscle cell (VSMC) migration an important trigger in development of atherosclerosis that associated with Chlamydia pneumoniae (C. pneumoniae) infection. However, the mechanism VSMC remains unclear, and whether antioxidant could be therapeutic target C. infection-induced also unknown. The results showed infection mainly impaired mitochondrial function increased level reactive oxygen species (mtROS). expressions protein JunB, Fra-1 Matrix metalloproteinase 2 (MMP) evidently after infection, interaction between JunB was enhanced. After scavenging mtROS by Mito-TEMPO, increasing Fra-1, MMP2 capacity induced were all inhibited. In comparison infected ApoE-/- mice, ROS atherosclerotic lesion ApoE-/-TLR2-/- mice decreased. Knocking out TLR2 suppressed VSMCs formation Furthermore, using small interfering RNA inhibit expression TLR2, apparently Taken together, may promote through activate JunB-Fra-1/MMP2 signaling pathway. data provide first evidence reduce atherosclerosis.