PMID- 35222713
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220301
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Print)
IS  - 1792-0981 (Linking)
VI  - 23
IP  - 3
DP  - 2022 Mar
TI  - Long non-coding RNA TUG1 sponges microRNA-9 to protect podocytes from high 
      glucose-induced apoptosis and mitochondrial dysfunction via SIRT1 upregulation.
PG  - 236
LID - 10.3892/etm.2022.11161 [doi]
LID - 236
AB  - Podocyte apoptosis and mitochondrial dysfunction serve a major role in diabetic 
      nephropathy progression. The present study revealed a molecular mechanism 
      regulating podocyte apoptosis and mitochondrial dysfunction. In vitro models were 
      established using conditionally immortalized mouse podocyte clonal cells treated 
      with high glucose (HG). Reverse quantitative-transcription PCR were used to 
      detect gene expression, western blotting and immunofluorescence were used to 
      detect protein expression, Cell Counting Kit-8 was used to detect cell viability 
      and flow cytometry was used to detect cell apoptosis. HG treatment in the mouse 
      podocyte clonal cells downregulated taurine-upregulated gene 1 (TUG1) expression 
      and decreased viability in a dose-dependent manner. In addition, TUG1 knockdown 
      (KD) increased HG-induced apoptosis, while TUG1 overexpression (OE) reduced 
      HG-induced apoptosis in podocytes. HG-induced mitochondrial dysfunction was 
      identified in podocytes, with increased reactive oxygen species levels, decreased 
      complex I/III activity and decreased basal/maximal oxygen consumption rate. TUG1 
      KD worsened HG-induced mitochondrial dysfunction, and TUG1 OE reversed these 
      effects. At the molecular level, TUG1 was revealed to promote sirtuin 1 (SIRT1) 
      expression by sponging microRNA (miR)-9, and SIRT1 OE reversed the HG-induced 
      apoptosis and mitochondrial dysfunction increased by TUG1 KD. The present data 
      indicated that downregulation of TUG1 induced by HG was associated with 
      HG-induced apoptosis and mitochondrial dysfunction in podocytes, and that TUG1 
      protected HG-induced podocytes by promoting SIRT1 expression via miR-9 
      inhibition.
CI  - Copyright: (c) Lei et al.
FAU - Lei, Min
AU  - Lei M
AD  - Department of Nephrology, Affiliated Hospital and Clinical Medical College of 
      Chengdu University, Jinniu, Chengdu, Sichuan 610081, P.R. China.
FAU - Ke, Guibao
AU  - Ke G
AD  - Department of Nephrology, Affiliated Hospital and Clinical Medical College of 
      Chengdu University, Jinniu, Chengdu, Sichuan 610081, P.R. China.
FAU - Wang, Yan
AU  - Wang Y
AD  - Department of Nephrology, Affiliated Hospital and Clinical Medical College of 
      Chengdu University, Jinniu, Chengdu, Sichuan 610081, P.R. China.
FAU - Luo, Dan
AU  - Luo D
AD  - Department of Nephrology, Affiliated Hospital and Clinical Medical College of 
      Chengdu University, Jinniu, Chengdu, Sichuan 610081, P.R. China.
FAU - Hu, Yao
AU  - Hu Y
AD  - Department of Nephrology, Affiliated Hospital and Clinical Medical College of 
      Chengdu University, Jinniu, Chengdu, Sichuan 610081, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20220124
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC8815052
OTO - NOTNLM
OT  - apoptosis
OT  - high glucose
OT  - mitochondrial dysfunction
OT  - podocytes
COIS- The authors declare that they have no competing interests.
EDAT- 2022/03/01 06:00
MHDA- 2022/03/01 06:01
PMCR- 2022/01/24
CRDT- 2022/02/28 05:35
PHST- 2021/04/01 00:00 [received]
PHST- 2021/09/16 00:00 [accepted]
PHST- 2022/02/28 05:35 [entrez]
PHST- 2022/03/01 06:00 [pubmed]
PHST- 2022/03/01 06:01 [medline]
PHST- 2022/01/24 00:00 [pmc-release]
AID - ETM-23-3-11161 [pii]
AID - 10.3892/etm.2022.11161 [doi]
PST - ppublish
SO  - Exp Ther Med. 2022 Mar;23(3):236. doi: 10.3892/etm.2022.11161. Epub 2022 Jan 24.