PMID- 25903459 OWN - NLM STAT- MEDLINE DCOM- 20160304 LR - 20181113 IS - 2047-783X (Electronic) IS - 0949-2321 (Print) IS - 0949-2321 (Linking) VI - 20 IP - 1 DP - 2015 Apr 23 TI - microRNA-98 mediated microvascular hyperpermeability during burn shock phase via inhibiting FIH-1. PG - 51 LID - 10.1186/s40001-015-0141-5 [doi] LID - 51 AB - BACKGROUND: microRNA is a small non-coding RNA molecule and functions in RNA silencing and post-transcriptional regulation of gene expression. This study was designed to evaluate the role of miR-98 in the development of microvascular permeability and its molecular pathogenesis. METHODS: Forty-eight healthy adult Wistar rats were divided into the control group (n = 8) and burn group (n = 40) that inflicted with 30% total body surface area third-degree burn. Groups were processed at 2, 4, 8, 12, and 24 h post-burn. Plasma for vascular endothelial cell culture was collected from control and 12 h post-burn rats. Organic microvascular permeability and serum miR-98 level were measured. In vitro, rat aorta endothelial cells were stimulated with burn serum. Level of miR-98 and protein of hypoxia-inducible factor-1 (HIF-1), factor inhibiting HIF-1alpha (FIH-1), and tight junction-associated proteins were determined. RESULTS: Organic microvascular permeability began to rise at 2 h post-burn and maintained the same character throughout the experiment except in lung tissue that was still rising at 12 h; the serum level of miR-98 was elevated (P < 0.05). In vitro, burn serum stimulation increased rat aorta endothelial monolayer cell permeability as well as upregulated miR-98 expression (P < 0.05). As shown in the result of transfection experiment, miR-98 negatively regulated FIH-1 and tight junction-associated protein expression (P < 0.05). CONCLUSIONS: The findings of the present study suggest severe microvascular permeability due to burns; and the underlying mechanism bases on the promotion of miR-98 level to the extent that it activated HIF-1 gene expression, resulting in junction-associated protein deficiency. FAU - Hu, Delin AU - Hu D AD - Department of Burns, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei, Anhui Province, 230022, People's Republic of China. Hu_del@163.com. FAU - Yu, Youxin AU - Yu Y AD - Department of Burns, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei, Anhui Province, 230022, People's Republic of China. Yyouxin@yeah.net. FAU - Wang, Chunhua AU - Wang C AD - Department of Burns, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei, Anhui Province, 230022, People's Republic of China. Chunh_w@126.com. FAU - Li, Denghui AU - Li D AD - Department of Burns, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei, Anhui Province, 230022, People's Republic of China. Ldengh@126.com. FAU - Tai, Yuncheng AU - Tai Y AD - Department of Burns, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei, Anhui Province, 230022, People's Republic of China. taiyunc@126.com. FAU - Fang, Linsen AU - Fang L AD - Department of Burns, The First Affiliated Hospital of Anhui Medical University, No. 218 Jixi Road, Hefei, Anhui Province, 230022, People's Republic of China. fangls@yeah.net. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20150423 PL - England TA - Eur J Med Res JT - European journal of medical research JID - 9517857 RN - 0 (Hif1a protein, rat) RN - 0 (Hypoxia-Inducible Factor 1, alpha Subunit) RN - 0 (MIRN98 microRNA-98, rat) RN - 0 (MicroRNAs) RN - 0 (Tight Junction Proteins) SB - IM MH - Animals MH - Burns/complications/*metabolism MH - *Capillary Permeability MH - Endothelium, Vascular/metabolism MH - Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism MH - MicroRNAs/*genetics MH - Microvessels/*metabolism MH - Rats MH - Rats, Wistar MH - Shock, Traumatic/etiology/*metabolism MH - Tight Junction Proteins/genetics/metabolism PMC - PMC4411771 EDAT- 2015/04/24 06:00 MHDA- 2016/03/05 06:00 PMCR- 2015/04/23 CRDT- 2015/04/24 06:00 PHST- 2015/01/06 00:00 [received] PHST- 2015/04/13 00:00 [accepted] PHST- 2015/04/24 06:00 [entrez] PHST- 2015/04/24 06:00 [pubmed] PHST- 2016/03/05 06:00 [medline] PHST- 2015/04/23 00:00 [pmc-release] AID - 10.1186/s40001-015-0141-5 [pii] AID - 141 [pii] AID - 10.1186/s40001-015-0141-5 [doi] PST - epublish SO - Eur J Med Res. 2015 Apr 23;20(1):51. doi: 10.1186/s40001-015-0141-5.