Long non-coding RNA TTC28-AS1 attenuates high glucose-induced damage in HK-2 cells depending on the regulation of miR-320a/CD2AP axis

Zhang Ji; Ding Juan; Yu Ming; Li Fang; Zhou Xue; Shuai Hongxia

doi:10.1007/s13258-021-01167-z

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자료유형: 학술저널

저자정보: Zhang Ji (Xiangyang Central Hospital China) Ding Juan (Xiangyang Central Hospital China) Yu Ming (Xiangyang Central Hospital China) Li Fang (Xiangyang Central Hospital China) Zhou Xue (Xiangyang Central Hospital China) Shuai Hongxia (Xiangyang Central Hospital China)

저널정보: 한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.12

발행연도: 2021.12

수록면: 1,471 - 1,482 (12page)

DOI: 10.1007/s13258-021-01167-z

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Background Diabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD) worldwide. Emerging evidence suggests that long non-coding RNAs (lncRNAs) play crucial roles in DN pathogenesis. Objective The purpose of the present study was to explore the role and mechanism of lncRNA tetratricopeptide repeat domain 2B antisense RNA 1 (TTC28-AS1) in DN. Methods Cell viability and apoptosis were assessed by the Cell Counting-8 Kit (CCK-8) assay and fow cytometry, respectively. The levels of TTC28-AS1, miR-320a and CD2-associated protein (CD2AP) were determined by quantitative real-time polymerase chain reaction (qRT-PCR) or western blot. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNFα), and IL-8 were gauged by enzyme-linked immunosorbent assay (ELISA). Targeted relationship between miR-320a and TTC28-AS1 or CD2AP was evaluated by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Results Our data indicated that high glucose (HG) induced HK-2 cell damage by the repression of cell viability and autophagy and the enhancement of cell apoptosis, fbrosis and pro-infammatory cytokines production. TTC28-AS1 was down-regulated and miR-320a was up-regulated in HG-induced HK-2 cells. TTC28-AS1 overexpression or miR-320a knockdown alleviated HG-induced damage in HK-2 cells. MiR-320 was a molecular mediator of TTC28-AS1 in regulating HG-induced HK-2 cell damage. Moreover, TTC28-AS1 functioned as a post-transcriptional regulator of CD2AP expression by miR-320a. MiR-320a knockdown relieved HG-induced damage in HK-2 cells by up-regulating CD2AP. Conclusions Our fndings suggest that TTC28-AS1 attenuates HG-induced damage in HK-2 cells at least partially by targeting the miR-320a/CD2AP axis, highlighting its role as a promising therapeutic approach for DN treatment.

#DN #TTC28-AS1 #miR-320a #CD2AP #Cell damage

참고문헌 (37)

참고문헌 신청

Bijkerk R / 2015 / Circulating microRNAs associate with diabetic nephropathy and systemic microvascular damage and normalize after simultaneous pancreas-kidney transplantation / Am J Transplant 15:1081~1090

Chen SJ / 2020 / Crosstalk between tubular epithelial cells and glomerular endothelial cells in diabetic kidney disease / Cell Prolif 53:e12763

Chen YQ / 2012 / Abated microRNA-195 expression protected mesangial cells from apoptosis in early diabetic renal injury in mice / J Nephrol 25:566~576

Conserva F / 2019 / Urinary miRNA-27b-3p and miRNA-1228-3p correlate with the progression of Kidney Fibrosis in Diabetic Nephropathy / Sci Rep 9:11357

Czajka A / 2016 / Hyperglycemia induced damage to mitochondrial respiration in renal mesangial and tubular cells : Implications for diabetic nephropathy / Redox Biol 10:100~107

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