PMID- 29852165
OWN - NLM
STAT- MEDLINE
DCOM- 20181126
LR  - 20210823
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 503
IP  - 1
DP  - 2018 Sep 3
TI  - T2DM inhibition of endothelial miR-342-3p facilitates angiogenic dysfunction via 
      repression of FGF11 signaling.
PG  - 71-78
LID - S0006-291X(18)31256-7 [pii]
LID - 10.1016/j.bbrc.2018.05.179 [doi]
AB  - Understanding the function and molecular relevance of distinct miRNAs in 
      endothelial cells (ECs) paves avenues for possible therapeutic intervention by 
      targeting epigenetic mechanisms in vascular endothelial dysfunction, one of the 
      major complications of type 2 diabetes mellitus (T2DM). MiR-342-3p, an 
      obesity-associated miRNA, has recently been shown to be significantly upregulated 
      in human angiosarcoma compared to benign hemangioma, indicating its potential 
      involvement as a proangiogenic factor. Herein, we show that endothelial 
      miR-342-3p expression was significantly compromised in T2DM organisms and this 
      inhibition powerfully blocked vasculogenesis in vivo by repressing endothelial 
      proliferation and migration. From a mechanistic standpoint, miR-342-3p promoted 
      the transactivation of fibroblast growth factor 11 (FGF11) by directly targeting 
      its 3' untranslated regions (3'UTRs). Functionally, overexpression of exogenous 
      FGF11 successfully rescued miR-342-3p deficiency-impaired endothelial 
      proliferation and migration. Thus, perturbation of miR-342-3p/FGF11 cascade by 
      hyperinsulinemia plays a causative role in the induction of vascular dysfunction 
      in T2DM. Overall, the current study underscore an endothelial facet of 
      miR-342-3p, which may operate as a novel epigenetic integrator linking adipogenic 
      homeostasis and angiogenesis.
CI  - Copyright (c) 2018 Elsevier Inc. All rights reserved.
FAU - Cheng, Shaoyun
AU  - Cheng S
AD  - Department of Clinical Laboratory, The 3(rd)People's Hospital of Qingdao, 
      Qingdao, 266041, Shandong Province, China.
FAU - Cui, Yanxiang
AU  - Cui Y
AD  - Department of Clinical Laboratory, Qingdao Huangdao District Hospital of 
      Traditional Chinese Medicine, Qingdao, 266500, Shandong Province, China.
FAU - Fan, Lin
AU  - Fan L
AD  - Department of Clinical Laboratory, The 3(rd)People's Hospital of Qingdao, 
      Qingdao, 266041, Shandong Province, China.
FAU - Mu, Xiaofeng
AU  - Mu X
AD  - Department of Clinical Laboratory, Qingdao Central Hospital, Qingdao, 266042, 
      Shandong Province, China.
FAU - Hua, Yuzhong
AU  - Hua Y
AD  - Department of Clinical Laboratory, The 3(rd)People's Hospital of Qingdao, 
      Qingdao, 266041, Shandong Province, China. Electronic address: hyz526@126.com.
LA  - eng
PT  - Journal Article
DEP - 20180607
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (3' Untranslated Regions)
RN  - 0 (FGF11 protein, human)
RN  - 0 (MIRN342 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (Mirn342 microRNA, mouse)
RN  - 0 (fibroblast growth factor 11, mouse)
RN  - 62031-54-3 (Fibroblast Growth Factors)
SB  - IM
MH  - 3' Untranslated Regions
MH  - Animals
MH  - Diabetes Mellitus, Experimental/genetics/pathology/physiopathology
MH  - Diabetes Mellitus, Type 2/*genetics/pathology/*physiopathology
MH  - Diabetic Angiopathies/genetics/pathology/physiopathology
MH  - Fibroblast Growth Factors/*genetics
MH  - Human Umbilical Vein Endothelial Cells
MH  - Humans
MH  - Hyperinsulinism/genetics/pathology/physiopathology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - MicroRNAs/antagonists & inhibitors/*genetics
MH  - Neovascularization, Pathologic/genetics/physiopathology
MH  - Signal Transduction
MH  - Transcriptional Activation
OTO - NOTNLM
OT  - Angiogenesis
OT  - Endothelial cells
OT  - FGF11
OT  - Hyperinsulinemia
OT  - miR-342-3p
EDAT- 2018/06/01 06:00
MHDA- 2018/11/27 06:00
CRDT- 2018/06/01 06:00
PHST- 2018/05/22 00:00 [received]
PHST- 2018/05/26 00:00 [accepted]
PHST- 2018/06/01 06:00 [pubmed]
PHST- 2018/11/27 06:00 [medline]
PHST- 2018/06/01 06:00 [entrez]
AID - S0006-291X(18)31256-7 [pii]
AID - 10.1016/j.bbrc.2018.05.179 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2018 Sep 3;503(1):71-78. doi: 
      10.1016/j.bbrc.2018.05.179. Epub 2018 Jun 7.