Identification of differentially expressed genes in mouse paraspinal muscle in response to microgravity

Author:

Li Yongjin,Kong Chao,Wang Baobao,Sun Wenzhi,Chen Xiaolong,Zhu Weiguo,Ding Junzhe,Lu Shibao

Abstract

Lower back pain (LBP) is the primary reason leading to dyskinesia in patients, which can be experienced by people of all ages. Increasing evidence have revealed that paraspinal muscle (PSM) degeneration (PSMD) is a causative contributor to LBP. Current research revealed that fatty infiltration, tissue fibrosis, and muscle atrophy are the characteristic pathological alterations of PSMD, and muscle atrophy is associated with abnormally elevated oxidative stress, reactive oxygen species (ROS) and inflammation. Interestingly, microgravity can induce PSMD and LBP. However, studies on the molecular mechanism of microgravity in the induction of PSMD are strongly limited. This study identified 23 differentially expressed genes (DEGs) in the PSM (longissimus dorsi) of mice which were flown aboard the Bion M1 biosatellite in microgravity by bioinformatics analysis. Then, we performed protein–protein interaction, Gene Ontology function, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis for the DEGs. We found that Il6ra, Tnfaip2, Myo5a, Sesn1, Lcn2, Lrg1, and Pik3r1 were inflammatory genes; Fbox32, Cdkn1a, Sesn1, and Mafb were associated with muscle atrophy; Cdkn1a, Sesn1, Lcn2, and Net1 were associated with ROS; and Sesn1 and Net1 were linked to oxidative stress. Furthermore, Lcn2, Fbxo32, Cdkn1a, Pik3r1, Sesn1, Net1, Il6ra, Myo5a, Lrg1, and Pfkfb3 were remarkably upregulated, whereas Tnfaip2 and Mafb were remarkably downregulated in PSMD, suggesting that they might play a significant role in regulating the occurrence and development of PSMD. These findings provide theoretical basis and therapeutic targets for the treatment of PSMD.

Publisher

Frontiers Media SA

Subject

Endocrinology, Diabetes and Metabolism

Cited by 3 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3