PMID- 30671964
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230201
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 234
IP  - 9
DP  - 2019 Sep
TI  - Deregulation of long noncoding RNA (TUG1) contributes to excessive podocytes 
      apoptosis by activating endoplasmic reticulum stress in the development of 
      diabetic nephropathy.
PG  - 15123-15133
LID - 10.1002/jcp.28153 [doi]
AB  - The objective of this study was to investigate the molecular mechanism of how 
      TUG1 interferes with the expression of C/EBP homologous protein (CHOP), 
      peroxisome-proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1alpha), which 
      contributes to the development of diabetic nephropathy. Real-time polymerase 
      chain reaction and western blot analysis were performed to explore the regulatory 
      relationship among TUG1, CHOP, PGC-1alpha, and caspase-3. Terminal deoxynucleotidyl 
      transferase dUTP nick-end labeling was performed to confirm TUG1 involved in 
      diabetic nephropathy (DN) through influencing podocytes apoptosis. TUG1 was 
      highly expressed in a cell following treatment with high glucose, and PGC-1alpha and 
      cleaved caspase-3 levels were much lower, while CHOP level was much higher in 
      high glucose group (HG), furthermore, CHOP inhibited PGC-1alpha expression. TUG1 
      negatively regulated CHOP expression, and positively regulated PGC-1alpha expression. 
      Meanwhile, total caspase-3 level in cell treated with or without HG transfected 
      with CHOP small interfering ribonucleic acid (siRNA), TUG1, and TUG1 siRNA showed 
      no evident difference with their corresponding control, while CHOP siRNA and TUG1 
      evidently decreased, and TUG1 siRNA remarkably increased cleaved caspase-3 level 
      in HG or normal glucose groups in comparison with corresponding control. TUG1 and 
      PGC-1alpha levels were much lower, while CHOP level was much higher in participants 
      diagnosed with DN. A higher level of CHOP protein and lower level of PGC-1alpha were 
      observed in subjects diagnosed with DN. Finally, podocytes apoptosis in the DN 
      group was significantly promoted compared with that in nondiabetic renal disease 
      group. Our current study has suggested for the first time that the long noncoding 
      RNA (lncRNA) TUG1 influenced podocytes apoptosis via mediating endoplasmic 
      reticulum stress (ERS)-CHOP-PGC-1alpha signaling pathway in HG-induced DN.
CI  - (c) 2019 Wiley Periodicals, Inc.
FAU - Shen, Hongchun
AU  - Shen H
AD  - Department of Nephrology, The Affiliated Traditional Medicine Hospital of 
      Southwest Medical University, Luzhou, Sichuan, China.
FAU - Ming, Yao
AU  - Ming Y
AD  - Department of Nephrology, The Affiliated Traditional Medicine Hospital of 
      Southwest Medical University, Luzhou, Sichuan, China.
FAU - Xu, Chuanlan
AU  - Xu C
AD  - Department of Nephrology, The Affiliated Traditional Medicine Hospital of 
      Southwest Medical University, Luzhou, Sichuan, China.
FAU - Xu, Yanwen
AU  - Xu Y
AD  - Department of Nephrology, The Affiliated Traditional Medicine Hospital of 
      Southwest Medical University, Luzhou, Sichuan, China.
FAU - Zhao, Sha
AU  - Zhao S
AD  - Department of Nephrology, The Affiliated Traditional Medicine Hospital of 
      Southwest Medical University, Luzhou, Sichuan, China.
FAU - Zhang, Qiong
AU  - Zhang Q
AUID- ORCID: 0000-0001-7916-6713
AD  - Department of Nephrology, The Affiliated Traditional Medicine Hospital of 
      Southwest Medical University, Luzhou, Sichuan, China.
LA  - eng
PT  - Journal Article
DEP - 20190122
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
SB  - IM
OTO - NOTNLM
OT  - CHOP
OT  - TUG1
OT  - apoptosis
OT  - diabetic nephropathy
OT  - endoplasmic reticulum stress
OT  - podocytes, PGC-1alpha
EDAT- 2019/01/24 06:00
MHDA- 2019/01/24 06:01
CRDT- 2019/01/24 06:00
PHST- 2018/11/11 00:00 [received]
PHST- 2018/12/18 00:00 [accepted]
PHST- 2019/01/24 06:00 [pubmed]
PHST- 2019/01/24 06:01 [medline]
PHST- 2019/01/24 06:00 [entrez]
AID - 10.1002/jcp.28153 [doi]
PST - ppublish
SO  - J Cell Physiol. 2019 Sep;234(9):15123-15133. doi: 10.1002/jcp.28153. Epub 2019 
      Jan 22.