Comparative proteomics profiling revealed the involvement of GRB2‐ROCK2 axis in Lyme neuroborreliosis caused by Borrelia Burgdorferi

The zoonotic Lyme neuroborreliosis (LNB) disease is caused by Borrelia burgdorferi, with wide distribution, rapid dissemination and high disability rate. However, the molecular mechanism underlying B. burgdorferi mediated neuroborreliosis remains largely unknown. Here, the frontal cortex from rhesus...

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Published in:Journal of cellular and molecular medicine Vol. 26; no. 8; pp. 2312 - 2321
Main Authors: Bi, Yunfeng, Liu, Jianjun, Ma, Mingbiao, Tao, Lvyan, Peng, Yun, Dai, Xiting, Ji, Zhenhua, Bai, Ruolan, Jian, Miaomiao, Chen, Taigui, Luo, Lisha, Wang, Feng, Ding, Zhe, Liu, Aihua, Bao, Fukai
Format: Journal Article
Language:English
Published: England John Wiley & Sons, Inc 01-04-2022
John Wiley and Sons Inc
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Summary:The zoonotic Lyme neuroborreliosis (LNB) disease is caused by Borrelia burgdorferi, with wide distribution, rapid dissemination and high disability rate. However, the molecular mechanism underlying B. burgdorferi mediated neuroborreliosis remains largely unknown. Here, the frontal cortex from rhesus brains was incubated with B. burgdorferi, and proteomics profiling was evaluated by isobaric tag for relative and absolute quantitation. Proteins were identified and quantified, and differentially expressed proteins (DEPs) were isolated by comparing co‐cultured samples and control samples. A total of 43, 164 and 368 DEPs were significantly altered after 6, 12 and 24 h treatment with B. burgdorferi respectively. Gene ontology and KEGG pathway analyses revealed that chemokine biological process was significantly enriched. Two genes in chemokine pathway including GRB2 and ROCK2 were significantly up‐regulated after B. burgdorferi co‐culturing. By in vitro assay, we confirmed that the expression of GRB2 and ROCK2 was increased after B. burgdorferi infection. In conclusion, our study revealed the involvement of chemokine pathway in the pathogenesis of LNB. GRB2 and ROCK2 may be novel biomarkers and therapeutic targets for LNB.
Bibliography:Funding information
Yunfeng Bi and Jianjun Liu are contributed equally to this work.
This study was supported by grants from the National Natural Science Foundation of China (Nos. 32060180, 81560596, and 81860644) and the Yunnan Applied Basic Research Projects (Nos. 2019FE001‐066 2019FE001‐002).
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ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.17253