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IF=6.08 | 恭贺赵茜科研团队使用HAKATA产品发表研究成果
更新时间:2022-08-15      阅读:911

(来源:论文截图)


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


发布期刊Frontiers in Cell and Developmental Biology

作者Xi Zhao1,2†, Guolin Miao1,3†, Lijun Zhang1†, Yuke Zhang1, Huanhuan Zhao1, Zhelong Xu1,Beibei Wang1* and Lijun Zhang1*

作者单位天津医科大学理生理学

DOI :doi.org/10.3389/fcell.2022.879023

引用试剂HAKATA  PBS缓冲液

影响因子:6.08

论文简述
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Infection is closely related to atherosclerosis, which is a major pathological basis for cardiovascular diseases. Vascular smooth muscle cell (VSMC) migration is an important trigger in development of atherosclerosis that is associated with Chlamydia pneumoniae (C. pneumoniae) infection. However, the mechanism of VSMC migration remains unclear, and whether antioxidant could be a therapeutic target for C. pneumoniae infection-induced atherosclerosis also remains unknown. The results showed that C. pneumoniae infection mainly impaired mitochondrial function and increased the level of mitochondrial reactive oxygen species (mtROS). The expressions of protein JunB, Fra-1 and Matrix metalloproteinase 2 (MMP) evidently increased after C. pneumoniae infection, and the interaction between JunB and Fra-1 was also enhanced. After scavenging mtROS by antioxidant Mito-TEMPO, the increasing expressions of JunB, Fra-1, MMP2 and the capacity of VSMC migration induced by C. pneumoniae infection were all inhibited. In comparison with infected ApoE mice, the level of ROS in atherosclerotic lesion in ApoETLR2 mice with C. pneumoniae infection decreased. Knocking out TLR2 suppressed the expressions of JunB, Fra-1 and MMP2 in VSMCs and the formation of atherosclerotic lesion after C. pneumoniae infection. Furthermore, after using small interfering RNA to inhibit the expression of TLR2, the level of mtROS and the expressions of JunB, Fra-1 and MMP2 apparently decreased. Taken together, C. pneumoniae infection may promote VSMC migration and atherosclerosis development by increasing the level of mtROS through TLR2 to activate the JunB-Fra-1/MMP2 signaling pathway. The data provide the first evidence that antioxidant could reduce C. pneumoniae infection-induced VSMC migration and atherosclerosis.

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使用产品
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在该研究过程中,科研团队研究人员使用了HAKATA的产品:

HAKATA PBS 缓冲液   (货号:A19711

能够为该研究提供助力,传秋生物/HAKATA深感荣幸。

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