PMID- 31489995
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230201
IS  - 1095-8355 (Electronic)
IS  - 1065-6995 (Linking)
VI  - 44
IP  - 1
DP  - 2020 Jan
TI  - LINC00462 is involved in high glucose-induced apoptosis of renal tubular 
      epithelial cells via AKT pathway.
PG  - 286-294
LID - 10.1002/cbin.11231 [doi]
AB  - New evidences suggest that long non-coding RNAs (lncRNAs) may play important 
      roles in a variety of kidney diseases, including diabetic nephropathy (DN). Our 
      present study investigated the potential function of LINC00462 in high glucose 
      (HG)-induced apoptosis of renal tubular epithelial cells (RTEC) and to determine 
      the underlying mechanism. The expression of LINC00462 in renal biopsy tissues was 
      examined using quantitative reverse-transcription polymerase chain reaction 
      (qRT-PCR). Then, a loss of function assay was performed to determine the 
      protective effect of LINC00462 in HG-induced RTEC damage. In addition, the 
      downstream signaling pathway of LINC00462 was also investigated. The qRT-PCR 
      results showed that the expression of LINC00462 was significantly up-regulated in 
      renal biopsies from DN patients. At the same time, LINC00462 was enhanced in a 
      glucose concentration- and time-dependent manner in human kidney (HK-2 and HKC) 
      cells subjected to HG treatment. The knockdown of LINC00462 improved the 
      significantly reduced cell viability of HG treatment, decreased HG-induced 
      reactive oxygen species (ROS) and malondialdehyde levels, and up-regulated the 
      response of antioxidant systems to ROS by increasing superoxide dismutase and 
      catalase levels. In addition, knockdown of LINC00462 inhibited HG-induced cell 
      apoptosis and affected the expression of apoptosis-related proteins. Most 
      importantly, we found that knockdown of LINC00462 enhanced the expression of 
      p-AKT. Moreover, AKT-specific inhibitor LY294002 restored the effect of LINC00462 
      knockdown on apoptosis. In conclusion, our study demonstrated that knockdown of 
      LINC00462 can ameliorate oxidative stress and apoptosis in HG-induced RTEC by 
      activating the AKT pathway, suggesting that knockdown of LINC00462 may provide a 
      potential therapeutic approach for DN.
CI  - (c) 2019 International Federation for Cell Biology.
FAU - Wang, Ruixin
AU  - Wang R
AD  - Department of Nephrology, The Fifth Affiliated Hospital of Guangzhou Medical 
      University, 621 Gangwan Road, Huangpu District, Guangzou, Guangdong, 510730, P.R. 
      China.
FAU - Yan, Yuehong
AU  - Yan Y
AD  - Department of Nephrology, The Fifth Affiliated Hospital of Guangzhou Medical 
      University, 621 Gangwan Road, Huangpu District, Guangzou, Guangdong, 510730, P.R. 
      China.
FAU - Li, Cuicui
AU  - Li C
AD  - Department of Nephrology, The Fifth Affiliated Hospital of Guangzhou Medical 
      University, 621 Gangwan Road, Huangpu District, Guangzou, Guangdong, 510730, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20190923
PL  - England
TA  - Cell Biol Int
JT  - Cell biology international
JID - 9307129
SB  - IM
OTO - NOTNLM
OT  - AKT signaling pathway
OT  - LINC00462
OT  - high glucose-induced apoptosis
OT  - renal tubular epithelial cells
EDAT- 2019/09/07 06:00
MHDA- 2019/09/07 06:01
CRDT- 2019/09/07 06:00
PHST- 2019/04/24 00:00 [received]
PHST- 2019/08/31 00:00 [accepted]
PHST- 2019/09/07 06:00 [pubmed]
PHST- 2019/09/07 06:01 [medline]
PHST- 2019/09/07 06:00 [entrez]
AID - 10.1002/cbin.11231 [doi]
PST - ppublish
SO  - Cell Biol Int. 2020 Jan;44(1):286-294. doi: 10.1002/cbin.11231. Epub 2019 Sep 23.