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microRNA-98 mediated microvascular hyperpermeability during burn shock phase via inhibiting FIH-1
Delin Hu1, Youxin Yu2, Chunhua Wang3
1Department 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.
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-1α (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.
Insights
Burn-induced microvascular permeability is exacerbated by elevated miR-98 levels. This microRNA promotes permeability by downregulating tight junction proteins, contributing to burn pathogenesis.
Area of Science:
- Biochemistry
- Molecular Biology
- Physiology
Background:
- MicroRNAs (miRNAs) are small non-coding RNAs regulating gene expression.
- This study investigates the role of miR-98 in burn-induced microvascular permeability.
Purpose of the Study:
- To evaluate the role of miR-98 in the development of microvascular permeability after burns.
- To elucidate the molecular pathogenesis of burn-induced microvascular hyperpermeability.
Main Methods:
- Wistar rats were subjected to third-degree burns and monitored for microvascular permeability and serum miR-98 levels.
- Rat aorta endothelial cells were stimulated with burn serum in vitro to assess miR-98 expression and cell permeability.
- Expression levels of hypoxia-inducible factor-1 (HIF-1), factor inhibiting HIF-1α (FIH-1), and tight junction proteins were determined.
Main Results:
- Microvascular permeability increased significantly post-burn, with elevated serum miR-98 levels.
- Burn serum stimulation in vitro increased endothelial cell permeability and miR-98 expression.
- miR-98 was found to negatively regulate FIH-1 and tight junction-associated proteins.
Conclusions:
- Elevated miR-98 levels contribute to severe microvascular permeability following burns.
- The mechanism involves miR-98 promoting HIF-1 gene expression, leading to tight junction protein deficiency.
