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收稿:2018-03-02,
纸质出版:2018-09-15
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魏毅, 于家伟, 张钧, 等. β-连环素互作蛋白1参与PPARγ转录活性调控及在高糖诱导系膜细胞表型转化中的作用[J]. 第三军医大学学报, 2018,40(17):1542-1547.
Yi WEI, Jiawei YU, Jun ZHANG, et al. Roles of ICAT in regulation of PPARγ transcriptional activity and phenotypic transition of human mesangial cells induced by high glucose[J]. Journal of Third Military Medical University, 2018, 40(17): 1542-1547.
魏毅, 于家伟, 张钧, 等. β-连环素互作蛋白1参与PPARγ转录活性调控及在高糖诱导系膜细胞表型转化中的作用[J]. 第三军医大学学报, 2018,40(17):1542-1547. DOI: 10.16016/j.1000-5404.201803011.
Yi WEI, Jiawei YU, Jun ZHANG, et al. Roles of ICAT in regulation of PPARγ transcriptional activity and phenotypic transition of human mesangial cells induced by high glucose[J]. Journal of Third Military Medical University, 2018, 40(17): 1542-1547. DOI: 10.16016/j.1000-5404.201803011.
Objective
2
To explore the roles of β-catenin-interacting protein 1 (ICAT) in regulating peroxisome proliferator-activated receptor gamma (PPARγ) transcriptional activity and inducing cell phenotypic transition in human mesangial cells (HMCs) cultured in high glucose (HG).
Methods
2
HMCs were cultured in either 5.5 (NC) or 30 (HG) mmol/L glucose medium. RT-PCR was used to detect the expression of PPARγ
ICAT and β-catenin in the cells. The protein levels of PPARγ
ICAT and β-catenin were detected by Western blotting. Cell phenotype transition of HMCs was detected by the expression levels of α-smooth muscular actin (α-SMA). And CCK-8 assay was used to measure cell proliferation.
Results
2
Compared with NC
HG induced the expression of α-SMA and promoted the proliferation of HMCs. Though HG showed no significant influence on PPARγ expression in HMCs (
P
>
0.05)
it lowered the transcriptional activity of PPARγ (
P
<
0.05)
inhibited the expression of ICAT but enhanced β-catenin. Over-expression of ICAT partially promoted the transcriptional activity of PPARγ (
P
<
0.05). Under normal glucose condition
knockdown of ICAT reduced the transcriptional activity of PPARγ (
P
<
0.01)
so was β-catenin knockdown (
P
<
0.01). However
under high glucose condition
over-expression of ICAT resulted in decreased expression of α-SMA and reduced proliferation of HMCs.
Conclusion
2
ICAT might be one of potential molecules in regulation of PPARγ transcriptional activity
and it also participates in mediating the cell phenotypic transition of HMCs induced by high glucose.
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