miR-495 Regulates Cellular Reactive Oxygen Species Levels by Targeting sod2 To Inhibit Intracellular Survival of Mycobacterium tuberculosis in Macrophages.
Xuanxiu RenWenqi DongJiajia FengPei LiYucheng ZhengGaoyan WangWenjia LuXiangru WangHuanchun ChenChen TanPublished in: Infection and immunity (2021)
Mycobacterium tuberculosis is a chronic infectious disease pathogen. To date, tuberculosis is a major infectious disease that endangers human health. To better prevent and treat tuberculosis, it is important to study the pathogenesis of M. tuberculosis. Based on early-stage laboratory research results, in this study, we verified the upregulation of sod2 in Bacillus Calmette-Guérin (BCG) and H37Rv infection. By detecting BCG/H37Rv intracellular survival in sod2-silenced and sod2-overexpressing macrophages, sod2 was found to promote the intracellular survival of BCG/H37Rv. miR-495 then was determined to be downregulated by BCG/H37Rv. BCG/H37Rv can upregulate sod2 expression by miR-495 to promote the intracellular survival of BCG/H37Rv through a decline in ROS levels. This study provides a theoretical basis for developing new drug targets and treating tuberculosis.
Keyphrases
- mycobacterium tuberculosis
- reactive oxygen species
- pulmonary tuberculosis
- cell proliferation
- early stage
- amyotrophic lateral sclerosis
- long non coding rna
- infectious diseases
- poor prognosis
- human health
- free survival
- dna damage
- cell death
- signaling pathway
- emergency department
- lymph node
- oxidative stress
- human immunodeficiency virus
- binding protein