PMID- 27363278 OWN - NLM STAT- MEDLINE DCOM- 20170103 LR - 20211203 IS - 1007-8738 (Print) IS - 1007-8738 (Linking) VI - 32 IP - 7 DP - 2016 Jul TI - [Overexpression of miR-125b promotes apoptosis of macrophages]. PG - 958-62 AB - Objective To investigate the expressions of miR-125b and target gene Raf1 proto-oncogene serine/threonine protein kinase (RAF1) in peripheral blood mononuclear cells (PBMCs) of pediatric patients with pulmonary tuberculosis (PTB), and observe the regulation of miR-125b on macrophage apoptosis and activity. Methods PBMCs of patients with PTB and healthy children were collected and separated. Real-time fluorescence quantitative PCR was used to detect mRNA expression level of miR-125b and RAF1, and Western blotting was used to detect the protein level of RAF1. THP-1 macrophages were transfected into miR-125b mimic, negative control mimic (NC-mimic), miR-125b inhibitor and negative control inhibitor (NC-inhibitor), which were cultured for 48 hours. Western blotting was performed to observe the expression of RAF1 in THP-1 macrophages, annexin V-FITC/PI double staining combined with flow cytometry was used to test cell apoptosis, and CCK-8 assay was used to detect cell proliferation. Results The expression of miR-125b in PBMCs in pediatric patients with PTB was downregulated, and mRNA and protein levels of RAF1 were upregulated. When miR-125b was over-expressed in THP-1 macrophages, the expression of RAF1 was reduced to promote the apoptosis of macrophages and decrease cell activity; when the expression of miR-125b was inhibited in THP-1 macrophages, the expression of RAF1 was elevatedand the apoptosis of macrophages was inhibited, the cell activity was promoted. Conclusion In PBMCs of children with PTB, miR-125b level is low. Upregulation of miR-125b in THP-1 macrophages, the apoptosis of THP-1 macrophages is promoted and cell activity is inhibited. FAU - Yu, Guangyuan AU - Yu G AD - Department of Gastroenterology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China. FAU - Zhan, Xue AU - Zhan X AD - Department of Gastroenterology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China. *Corresponding authors, E-mail: zhanxue@hotmail.com. FAU - Zhang, Zhenzhen AU - Zhang Z AD - Department of Infection, Children's Hospital of Chongqing Medical University, Chongqing 400014, China. *Corresponding authors, E-mail: 39003614@qq.com. FAU - Li, Yasha AU - Li Y AD - Pediatrics Research Institute, Children's Hospital of Chongqing Medical University, Ministry-of-Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing 400014, China. LA - chi PT - Journal Article PL - China TA - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi JT - Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology JID - 101139110 RN - 0 (MAS1 protein, human) RN - 0 (MIRN125 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (Proto-Oncogene Mas) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-raf) SB - IM MH - Adolescent MH - Apoptosis/*genetics MH - Blotting, Western MH - Cell Line, Tumor MH - Cells, Cultured MH - Child MH - Child, Preschool MH - Female MH - Flow Cytometry MH - *Gene Expression MH - Humans MH - Infant MH - Infant, Newborn MH - Leukocytes, Mononuclear/metabolism MH - Macrophages/*metabolism MH - Male MH - MicroRNAs/*genetics MH - Proto-Oncogene Mas MH - Proto-Oncogene Proteins c-raf/*genetics/metabolism MH - Reverse Transcriptase Polymerase Chain Reaction MH - Tuberculosis, Pulmonary/blood/genetics/metabolism EDAT- 2016/07/02 06:00 MHDA- 2017/01/04 06:00 CRDT- 2016/07/02 06:00 PHST- 2016/07/02 06:00 [entrez] PHST- 2016/07/02 06:00 [pubmed] PHST- 2017/01/04 06:00 [medline] PST - ppublish SO - Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2016 Jul;32(7):958-62.