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miR-186-5p负性调控CDCA3对高脂高糖诱导的胰岛β细胞具有保护作用
MiR-186-5p negatively regulates CDCA3 to improve proliferation and inhibit apoptosis of islet β cells induced by high fat and high glucose
- 第三军医大学学报 2020年42卷第19期 页码：1930-1937
- 作者机构：
- 作者简介：
- 基金信息：
DOI：10.16016/j.1000-5404.202003247
中图分类号：收稿：2020-03-19，
纸质出版：2020-10-15
- 稿件说明：
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翟铁, 田雪品, 郝凤杰, 等. miR-186-5p负性调控CDCA3对高脂高糖诱导的胰岛β细胞具有保护作用[J]. 第三军医大学学报, 2020,42(19):1930-1937.
Tie ZHAI, Xuepin TIAN, Fengjie HAO, et al. MiR-186-5p negatively regulates CDCA3 to improve proliferation and inhibit apoptosis of islet β cells induced by high fat and high glucose[J]. Journal of Third Military Medical University, 2020, 42(19): 1930-1937.
翟铁, 田雪品, 郝凤杰, 等. miR-186-5p负性调控CDCA3对高脂高糖诱导的胰岛β细胞具有保护作用[J]. 第三军医大学学报, 2020,42(19):1930-1937. DOI： 10.16016/j.1000-5404.202003247.
Tie ZHAI, Xuepin TIAN, Fengjie HAO, et al. MiR-186-5p negatively regulates CDCA3 to improve proliferation and inhibit apoptosis of islet β cells induced by high fat and high glucose[J]. Journal of Third Military Medical University, 2020, 42(19): 1930-1937. DOI： 10.16016/j.1000-5404.202003247.
摘要
Abstract
Objective
2
To investigate whether miR-186-5p can regulate the proliferation and apoptosis of islet β-cells induced by high fat and high glucose through cell division cycle associated 3 protein (CDCA3).
Methods
2
Mouse pancreatic β-cell line NIT-1 was treated with high lipid and glucose to induce injury. CCK-8 assay and flow cytometry were employed to measure cell proliferation and apoptosis. The expression of Ki-67
PCNA
Bcl-2 and Bax at protein level was analyzed by Western blotting
while that of miR-186-5p and CDCA3 at mRNA level was determined by qRT-PCR. Bioinformatics and dual luciferase activity assay were used to predict and detect the targeting relationship between miR-186-5p and CDCA3. NIT-1 cells were transfected with miR-186-5p or si-CDCA3
and treated with high lipid and high glucose
and the effects on cell proliferation and apoptosis were observed.
Results
2
High lipid and high glucose significantl
y reduced the cell viability
protein levels of Ki-67
PCNA and Bcl-2
and mRNA level of miR-186-5p expression in NIT-1 cells
while significantly increased the cell apoptotic rate and Bax protein expression
as well as CDCA3 expression at mRNA and protein levels (
P
<
0.05). MiR-186-5p negatively regulates CDCA3 as a target. Overexpression of miR-186-5p or knockdown of CDCA3 dramatically improved the cell viability
increased the expression of Ki-67
PCNA
and Bcl-2 at protein level
while remarkably decreased the apoptotic rate and Bax protein expression in NIT-1 cells after the treatment of high lipid and high glucose (
P
<
0.05).
Conclusion
2
ConclusionmiR-186-5p can negatively regulate the expression of CDCA3 gene
and thus promote the proliferation of islet β cells induced by high fat and high glucose and inhibit the apoptosis
so as to protect the islet β cells against the damage induced by high fat and high glucose.
关键词
Keywords
references
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