PMID- 34649592
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211022
IS  - 1758-5996 (Print)
IS  - 1758-5996 (Electronic)
IS  - 1758-5996 (Linking)
VI  - 13
IP  - 1
DP  - 2021 Oct 14
TI  - CDKN2B-AS1 participates in high glucose-induced apoptosis and fibrosis via NOTCH2 
      through functioning as a miR-98-5p decoy in human podocytes and renal tubular 
      cells.
PG  - 107
LID - 10.1186/s13098-021-00725-5 [doi]
LID - 107
AB  - BACKGROUND: Diabetic nephropathy (DN) is the most common causes of end-stage 
      renal disease. Long non-coding RNA cyclin-dependent kinase inhibitor 2B antisense 
      RNA 1 (CDKN2B-AS1) is connected with the development of DN, but the role of 
      CDKN2B-AS1 in DN has not been entirely elucidated. METHODS: Quantitative 
      real-time polymerase chain reaction (qRT-PCR) was carried out to measure 
      CDKN2B-AS1 and miR-98-5p levels. Cell viability, proliferation, and apoptosis 
      were analyzed with 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide 
      (MTT) or flow cytometry assays. Protein levels were measured by western blotting. 
      The relationship between CDKN2B-AS1 or notch homolog 2 (NOTCH2) and miR-98-5p was 
      verified via dual-luciferase reporter assay. RESULTS: CDKN2B-AS1 and NOTCH2 were 
      upregulated in the serum of DN patients and high glucose-disposed human podocytes 
      (HPCs) and human renal tubular cells (HK-2), whereas miR-98-5p was downregulated. 
      High glucose repressed viability and accelerated apoptosis of HPCs and HK-2 
      cells. CDKN2B-AS1 knockdown impaired high glucose-induced apoptosis and fibrosis 
      of HPCs and HK-2 cells. Mechanistically, CDKN2B-AS1 sponged miR-98-5p to regulate 
      NOTCH2 expression. Also, CDKN2B-AS1 inhibition-mediated effects on apoptosis and 
      fibrosis of high glucose-disposed HPCs and HK-2 cells were weakened by miR-98-5p 
      inhibitor. Also, NOTCH2 knockdown partly reversed miR-98-5p inhibitor-mediated 
      impacts on apoptosis and fibrosis of high glucose-disposed HPCs and HK-2 cells. 
      CONCLUSION: High glucose-induced CDKN2B-AS1 promoted apoptosis and fibrosis via 
      the TGF-beta1 signaling mediated by the miR-98-5p/NOTCH2 axis in HPCs and HK-2 
      cells.
CI  - (c) 2021. The Author(s).
FAU - Xiao, Min
AU  - Xiao M
AD  - Department of Nephrology, Qilu Hospital, Cheeloo College of Medicine, Shandong 
      University, 107 Wenhua West Road, Jinan, 250012, Shandong, China.
FAU - Bai, Shoujun
AU  - Bai S
AD  - Department of Nephrology, Qingpu Branch of Zhongshan Hospital Affiliated To Fudan 
      University, Shanghai, 201700, China.
FAU - Chen, Jing
AU  - Chen J
AD  - School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, 750004, 
      China.
FAU - Li, Yaxi
AU  - Li Y
AD  - Department of Biomedical Engineering, University of Houston, Houston, TX, 77004, 
      USA.
FAU - Zhang, Shu
AU  - Zhang S
AD  - Department of Biomedical Engineering, University of Houston, Houston, TX, 77004, 
      USA.
FAU - Hu, Zhao
AU  - Hu Z
AD  - Department of Nephrology, Qilu Hospital, Cheeloo College of Medicine, Shandong 
      University, 107 Wenhua West Road, Jinan, 250012, Shandong, China. 
      min_xiao_1017@126.com.
LA  - eng
PT  - Journal Article
DEP - 20211014
PL  - England
TA  - Diabetol Metab Syndr
JT  - Diabetology & metabolic syndrome
JID - 101488958
PMC - PMC8518318
OTO - NOTNLM
OT  - CDKN2B-AS1
OT  - DN
OT  - NOTCH2
OT  - miR-98-5p
COIS- The authors declare that they have no competing interests.
EDAT- 2021/10/16 06:00
MHDA- 2021/10/16 06:01
PMCR- 2021/10/14
CRDT- 2021/10/15 05:29
PHST- 2021/04/03 00:00 [received]
PHST- 2021/09/24 00:00 [accepted]
PHST- 2021/10/15 05:29 [entrez]
PHST- 2021/10/16 06:00 [pubmed]
PHST- 2021/10/16 06:01 [medline]
PHST- 2021/10/14 00:00 [pmc-release]
AID - 10.1186/s13098-021-00725-5 [pii]
AID - 725 [pii]
AID - 10.1186/s13098-021-00725-5 [doi]
PST - epublish
SO  - Diabetol Metab Syndr. 2021 Oct 14;13(1):107. doi: 10.1186/s13098-021-00725-5.