The Favored Mechanism for Coping with Acute Cold Stress: Upregulation of miR-210 in Rats
| Autor: | Li-Ping Zhang, Jianfa Wang, Shuai Lian, Hong Ji, Huanmin Yang, Shucheng Zang, Jingru Guo, Wenjin Guo, Limin Lang, Li Zhen, Yan Chen, Bin Xu, Shoupeng Fu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
Male
0301 basic medicine Cell death Programmed cell death Physiology Acclimatization Cell Proliferation lcsh:Physiology Cell Line miR-210 lcsh:Biochemistry 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Gene expression medicine Animals lcsh:QD415-436 Rats Wistar biology lcsh:QP1-981 Cell growth Chemistry Cold-Shock Response Transfection Molecular biology Mitochondria Rats Up-Regulation Cold Temperature MicroRNAs 030104 developmental biology medicine.anatomical_structure Gene Expression Regulation Apoptosis biology.protein ISCU Cold stress Glycolysis 030217 neurology & neurosurgery Mitochondrial respiration |
| Zdroj: | Cellular Physiology and Biochemistry, Vol 46, Iss 5, Pp 2090-2102 (2018) |
| ISSN: | 1421-9778 1015-8987 |
| Popis: | Background/Aims: The main aim of this study was to determine the mechanisms by which rno-miR-210-3p affects changes in gene expression, metabolism, apoptosis and proliferation of cells under acute cold stress (ACS) conditions. Methods: The treatment group (n=6, weight 340±20 g) was exposed to ACS (temperature 4±0.5°C, relative humidity 45±0.5%) and the control group (n=6, weight 340±20 g) to normal temperature (NT) (temperature 24±0.5°C, relative humidity 45±0.5%). Rat liver samples were collected for qRT-PCR and western blot analyses to detect relative expression of rno-miR-210-3p, ISCU, Rap1b, ATP1b1, GPD1, E2F3, RAD52, PSMB6 and GPD2. For cell experiments, 100 pmol/dish rno-miR-210-3p mimic and 150 pmol/dish rno-miR-210-3p inhibitor were used. Mitochondrial glucose flux and glycolysis were measured using the XFe24 Extracellular Flux Analyzer. Cells were collected for apoptosis analysis 24 h after transfection and proliferation was quantified using the WST-1 Cell Proliferation and Cytotoxicity Assay Kit (Beyotime, Shanghai, China), according to the manufacturerʹs instructions. Results: In the rat experiment, expression of rno-miR-210-3p under ACS was increased sharply while ISCU, E2F3, RAD52, and PSMB6 levels declined, along with protein expression of ISCU and PSMB6. In cell experiments, ISCU, Rap1b, ATP1b1, GPD1, E2F3, RAD52, PSMB6 and GPD2 genes were downregulated while ISCU and PSMB6 protein expression decreased with upregulation of rno-miR-210-3p. Conversely, in response to decreased rno-miR-210-3p expression, ISCU, E2F3, RAD52, PSMB6 and GPD2 genes were upregulated, in addition to ISCU and PSMB6 proteins. Upregulation of miR-210 inhibited cell proliferation and induced cell death whereas its downregulation promoted cell proliferation. Upregulation or downregulation of miR-210 promoted glycolysis and mitochondrial respiration of BRL cells. However, downregulation of miR-210 caused acid production in cells. Conclusion: Expression of rno-miR-210-3p is significantly increased under ACS. Upregulation of rno-miR-210-3p inhibits the expression of ISCU, Rap1b, ATP1b1, GPD1, E2F3, RAD52, PSMB6 and GPD2 genes, promotes glycolysis of liver and enhances the mitochondrial respiratory capacity of cells, but may also cause cell death. Our findings collectively indicate that regulation of rno-miR-210-3p is a preferential mechanism of choice used by the body to cope with ACS. |
| Databáze: | OpenAIRE |
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