PMID- 32726814
OWN - NLM
STAT- MEDLINE
DCOM- 20220307
LR  - 20220307
IS  - 1439-3646 (Electronic)
IS  - 0947-7349 (Linking)
VI  - 130
IP  - 1
DP  - 2022 Jan
TI  - Knock-Down of Long Non-Coding RNA ANRIL Suppresses Mouse Mesangial Cell 
      Proliferation, Fibrosis, Inflammation via Regulating Wnt/beta-Catenin and MEK/ERK 
      Pathways in Diabetic Nephropathy.
PG  - 30-36
LID - 10.1055/a-1185-9283 [doi]
AB  - AIMS: Our study aimed to investigate the role of long non-coding RNA ANRIL 
      (lnc-ANRIL) knock-down in regulating cell activities, inflammation and downstream 
      signaling pathways in mouse mesangial cellular diabetic nephropathy (DN) model.: 
      METHODS: The mouse mesangial cells (SV40-MES13 cells) were treated with 
      high-glucose (HG) to construct cellular DN model. Lnc-ANRIL knock-down plasmid 
      and control knock-down plasmid were transfected into HG-treated SV40-MES13 cells 
      as Sh-ANRIL group and Sh-NC group respectively. RESULTS: Lnc-ANRIL expression was 
      significantly higher in HG-treated SV40-MES13 cells compared with normal 
      glucose-treated SV40-MES13 cells and osmotic control-treated SV40-MES13 cells. 
      Lnc-ANRIL knock-down suppressed cell proliferation and promoted cell apoptosis in 
      HG-treated SV40-MES13 cells. As for fibrosis, lnc-ANRIL knock-down reduced 
      fibronectin and collagen I expressions in HG-treated SV40-MES13 cells. Besides, 
      the expressions of supernatant tumor necrosis factor-alpha (TNF-alpha), monocyte 
      chemoattractant protein-1 (MCP-1), interleukin (IL)-1beta, IL-6, IL-8 and IL-18 were 
      reduced in Sh-ANRIL group compared with Sh-NC group. Furthermore, Wnt3, 
      beta-catenin, p-MEK1 and p-ERK1 expressions were suppressed in Sh-ANRIL group 
      compared with Sh-NC group, which suggested that lnc-ANRIL knock-down inhibited 
      Wnt/beta-catenin and MEK/ERK pathways in HG-treated SV40-MES13 cells. CONCLUSIONS: 
      Lnc-ANRIL knock-down suppresses mouse mesangial cell proliferation, fibrosis, 
      inflammation, Wnt/beta-catenin and MEK/ERK pathways in DN.
CI  - Thieme. All rights reserved.
FAU - Fang, Xun
AU  - Fang X
AD  - Department of Nephrology, The Central Hospital of Wuhan, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, P. R. China.
FAU - Hu, Jun
AU  - Hu J
AD  - Department of Gerontology, The Central Hospital of Wuhan, Tongji Medical College, 
      Huazhong University of Science and Technology, Wuhan, P. R. China.
FAU - Zhou, Hongyan
AU  - Zhou H
AD  - Department of Endocrinology, The Central Hospital of Wuhan, Tongji Medical 
      College, Huazhong University of Science and Technology, Wuhan, P. R. China.
LA  - eng
PT  - Journal Article
DEP - 20200729
PL  - Germany
TA  - Exp Clin Endocrinol Diabetes
JT  - Experimental and clinical endocrinology & diabetes : official journal, German 
      Society of Endocrinology [and] German Diabetes Association
JID - 9505926
RN  - 0 (RNA, Long Noncoding)
SB  - IM
MH  - Animals
MH  - Cell Proliferation/physiology
MH  - Diabetic Nephropathies/*metabolism
MH  - Fibrosis
MH  - Inflammation/*metabolism
MH  - *MAP Kinase Signaling System
MH  - Mesangial Cells/*physiology
MH  - Mice
MH  - RNA, Long Noncoding/*metabolism
MH  - *Wnt Signaling Pathway
COIS- The authors declare that they have no conflict of interest.
EDAT- 2020/07/30 06:00
MHDA- 2022/03/08 06:00
CRDT- 2020/07/30 06:00
PHST- 2020/07/30 06:00 [pubmed]
PHST- 2022/03/08 06:00 [medline]
PHST- 2020/07/30 06:00 [entrez]
AID - 10.1055/a-1185-9283 [doi]
PST - ppublish
SO  - Exp Clin Endocrinol Diabetes. 2022 Jan;130(1):30-36. doi: 10.1055/a-1185-9283. 
      Epub 2020 Jul 29.