PMID- 35278152 OWN - NLM STAT- MEDLINE DCOM- 20220425 LR - 20221005 IS - 1559-0283 (Electronic) IS - 1085-9195 (Linking) VI - 80 IP - 2 DP - 2022 Jun TI - MicroRNA-629-3p Promotes Interleukin-13-Induced Bronchial Epithelial Cell Injury and Inflammation by Targeting FOXA2. PG - 457-466 LID - 10.1007/s12013-022-01072-6 [doi] AB - OBJECTIVE: Asthma is a chronic pulmonary inflammatory disease. MicroRNA (miR)-629-3p expression is reported to be up-regulated in the sputum of asthma patients. Nonetheless, miR-629-3p's role and mechanism in asthma remain largely unknown. This study is aimed at exploring miR-629-3p's role in regulating the injury and inflammation of bronchial epithelial cells. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to detect the expression levels of miR-629-3p and forkhead box a2 (FOXA2) mRNA in 16HBE cells treated with interleukin-13 (IL-13). 16HBE cell viability was evaluated using the cell counting kit-8 (CCK-8) assay, and cell apoptosis was analyzed by a flow cytometer. The levels of C-C motif chemokine ligand 11 (CCL11), C-C motif chemokine ligand 26 (CCL26), C-C motif ligand 2 (CCL-2)/mono-cyte chemotactic protein-1 (MCP-1), interleukin-1 beta (IL-1b), and interleukin 6 (IL-6) in 16HBE cell supernatant were detected through enzyme-linked immunosorbent assay (ELISA). The downstream target genes of miR-629-3p were predicted through bioinformatics. Besides, the targeted relationship between miR-629-3p and FOXA2 mRNA 3'-UTR was verified by dual-luciferase reporter gene assay. Western blot was utilized to determine the regulatory effects of miR-629-3p on the expression of FOXA2 protein in 16HBE cells. RESULTS: MiR-629-3p expression was significantly enhanced in IL-13-stimulated 16HBE cells while the FOXA2 mRNA and protein levels were significantly down-regulated. The transfection of miR-629-3p mimics inhibited 16HBE cells' viability, and promoted the apoptosis and the secretion of chemokines CCL11, CCL26, CCL-2/MCP-1, IL-1b, and IL-6 of 16HBE cells, whereas inhibiting miR-629-3p had the opposite effects. Moreover, FOXA2 was identified as a downstream miR-629-3p target, and its overexpression reversed the effects of the miR-629-3p on 16HBE cells. CONCLUSION: MiR-629-3p promotes IL-13-induced 16HBE cells' injury and inflammation by targeting FOXA2. CI - (c) 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. FAU - Jian, Guo AU - Jian G AD - Department of Intensive Care Unit, The Lihuili Affiliated Hospital, Ningbo University, Ningbo, Zhejiang, China. FAU - Yangli, Jin AU - Yangli J AD - Department of Ultrasound, Yinzhou No. 2 Hospital, Ningbo, Zhejiang, China. 553814675@qq.com. FAU - Chao, Zhang AU - Chao Z AD - Department of Pediatrics, Xi'an No. 3 Hospital, Xi'an, Shaanxi, China. FAU - Kun, Wang AU - Kun W AD - Department of Pediatrics, Xi'an No. 3 Hospital, Xi'an, Shaanxi, China. FAU - Xiaomin, Zhang AU - Xiaomin Z AUID- ORCID: 0000-0001-9146-2849 AD - Department of Pediatrics, Xi'an No. 3 Hospital, Xi'an, Shaanxi, China. drzhangxm@21cn.com. LA - eng PT - Journal Article DEP - 20220312 PL - United States TA - Cell Biochem Biophys JT - Cell biochemistry and biophysics JID - 9701934 RN - 0 (Chemokines) RN - 0 (FOXA2 protein, human) RN - 0 (Interleukin-13) RN - 0 (Interleukin-6) RN - 0 (Ligands) RN - 0 (MIRN629 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (RNA, Messenger) RN - 135845-92-0 (Hepatocyte Nuclear Factor 3-beta) SB - IM MH - Apoptosis/genetics MH - *Asthma/metabolism MH - Chemokines/adverse effects/metabolism MH - Epithelial Cells/metabolism MH - Hepatocyte Nuclear Factor 3-beta/genetics/metabolism MH - Humans MH - Inflammation/chemically induced/genetics/metabolism MH - Interleukin-13/adverse effects/pharmacology MH - Interleukin-6/metabolism MH - Ligands MH - *MicroRNAs/genetics/metabolism MH - RNA, Messenger/genetics/metabolism OTO - NOTNLM OT - Asthma OT - Cell damage OT - FOXA2 OT - Inflammation OT - MiR-629-3p EDAT- 2022/03/13 06:00 MHDA- 2022/04/26 06:00 CRDT- 2022/03/12 12:07 PHST- 2021/05/11 00:00 [received] PHST- 2022/02/14 00:00 [accepted] PHST- 2022/03/13 06:00 [pubmed] PHST- 2022/04/26 06:00 [medline] PHST- 2022/03/12 12:07 [entrez] AID - 10.1007/s12013-022-01072-6 [pii] AID - 10.1007/s12013-022-01072-6 [doi] PST - ppublish SO - Cell Biochem Biophys. 2022 Jun;80(2):457-466. doi: 10.1007/s12013-022-01072-6. Epub 2022 Mar 12.