PMID- 32905431
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220416
IS  - 1758-5996 (Print)
IS  - 1758-5996 (Electronic)
IS  - 1758-5996 (Linking)
VI  - 12
DP  - 2020
TI  - LncRNA KCNQ1OT1 affects cell proliferation, apoptosis and fibrosis through 
      regulating miR-18b-5p/SORBS2 axis and NF-kB pathway in diabetic nephropathy.
PG  - 77
LID - 10.1186/s13098-020-00585-5 [doi]
LID - 77
AB  - BACKGROUND: It has been reported that long non-coding RNAs (lncRNAs) play vital 
      roles in diabetic nephropathy (DN). Our study aims to research the function of 
      lncRNA KCNQ1OT1 in DN cells and the molecular mechanism. METHODS: Human 
      glomerular mesangial cells (HGMCs) and human renal glomerular endothelial cells 
      (HRGECs) were cultured in high glucose (30 mM) condition as models of DN cells. 
      KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) and miR-18b-5p levels 
      were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The 
      mRNA and protein levels of Sorbin and SH3 domain-containing protein 2 (SORBS2), 
      Type IV collagen (Col-4), fibronectin (FN), transcriptional regulatory 
      factor-beta 1 (TGF-beta1), Twist, NF-kappaB and STAT3 were measured by qRT-PCR and 
      western blot. Cell viability was detected by cell counting kit-8 (CCK-8) assay 
      for selecting the proper concentration of glucose treatment. Additionally, 
      3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) and flow 
      cytometry assay were employed to determine cell proliferation and apoptosis, 
      respectively. The targets of KCNQ1OT1 was predicted by online software and 
      confirmed by dual-luciferase reporter assay. RESULTS: KCNQ1OT1 and SORBS2 were 
      elevated in DN. Both knockdown of KCNQ1OT1 and silencing of SORBS2 restrained 
      proliferation and fibrosis and induced apoptosis in DN cells. Besides, 
      Overexpression of SORBS2 restored the KCNQ1OT1 knockdown-mediate effects on 
      proliferation, apoptosis and fibrosis in DN cells. In addition, miR-18b-5p served 
      as a target of KCNQ1OT1 as well as targeted SORBS2. KCNQ1OT1 knockdown repressed 
      NF-kB pathway. CONCLUSION: KCNQ1OT1 regulated DN cells proliferation, apoptosis 
      and fibrosis via KCNQ1OT1/miR-18b-5p/SORBS2 axis and NF-kB pathway.
CI  - (c) The Author(s) 2020.
FAU - Jie, Ran
AU  - Jie R
AD  - Department of Endocrinology, First People's Hospital of Jingzhou, Shashi 
      District, No. 8 Hangkong Road, Jingzhou, 434000 Hubei China. GRID: grid.459509.4
FAU - Zhu, Pengpeng
AU  - Zhu P
AD  - Department of Anesthesiology, First People's Hospital of Jingzhou, Jingzhou, 
      434000 Hubei China. GRID: grid.459509.4
FAU - Zhong, Jiao
AU  - Zhong J
AD  - Health Management Center, First People's Hospital of Jingzhou, Jingzhou, 434000 
      Hubei China. GRID: grid.459509.4
FAU - Zhang, Yan
AU  - Zhang Y
AD  - Department of Gastroenterology, First People's Hospital of Jingzhou, Jingzhou, 
      434000 Hubei China. GRID: grid.459509.4
FAU - Wu, Hongyan
AU  - Wu H
AD  - Department of Endocrinology, First People's Hospital of Jingzhou, Shashi 
      District, No. 8 Hangkong Road, Jingzhou, 434000 Hubei China. GRID: grid.459509.4
LA  - eng
PT  - Journal Article
DEP - 20200903
PL  - England
TA  - Diabetol Metab Syndr
JT  - Diabetology & metabolic syndrome
JID - 101488958
PMC - PMC7469295
OTO - NOTNLM
OT  - Diabetic nephropathy
OT  - KCNQ1OT1
OT  - NF-kB pathway
OT  - SORBS2
OT  - miR-18b-5p
COIS- Competing interestsThe authors declare that they have no competing interests.
EDAT- 2020/09/10 06:00
MHDA- 2020/09/10 06:01
PMCR- 2020/09/03
CRDT- 2020/09/09 18:14
PHST- 2020/05/21 00:00 [received]
PHST- 2020/08/21 00:00 [accepted]
PHST- 2020/09/09 18:14 [entrez]
PHST- 2020/09/10 06:00 [pubmed]
PHST- 2020/09/10 06:01 [medline]
PHST- 2020/09/03 00:00 [pmc-release]
AID - 585 [pii]
AID - 10.1186/s13098-020-00585-5 [doi]
PST - epublish
SO  - Diabetol Metab Syndr. 2020 Sep 3;12:77. doi: 10.1186/s13098-020-00585-5. 
      eCollection 2020.