PMID- 30149681
OWN - NLM
STAT- MEDLINE
DCOM- 20181211
LR  - 20181211
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 19
IP  - 9
DP  - 2018 Aug 26
TI  - Ghrelin Stimulates Endothelial Cells Angiogenesis through Extracellular Regulated 
      Protein Kinases (ERK) Signaling Pathway.
LID - 10.3390/ijms19092530 [doi]
LID - 2530
AB  - Adipose tissue is hyper-vascularized. Vessels in adipose tissue not only supply 
      nutrients and oxygen to nourish adipocytes, but also provide cytokines that 
      regulate mass and function of adipose tissue. Understanding the fundamental 
      mechanisms how vessels modulate adipocyte functions would provide new therapeutic 
      options for treatment of metabolic disease and obesity. In recent years, 
      researches about ghrelin are focused on glucose and lipid metabolism, but its 
      effect on vascular function remains uncharacterized. In the present study, 
      ghrelin receptor gene deletion mice (Ghsr(-/-) mice) were used to study 
      ghrelin-regulated vascular metabolism in white adipose tissue. Ghsr(-/-) mice 
      demonstrated lower food intake, lower body weight, and resistance to high-fat 
      diet-induced obesity. The number of vessels in white adipose tissue was decreased 
      in Ghsr(-/-) mice when compared with wild type mice fed with high-fat diet. To 
      further define ghrelin effects in vitro, we used endothelial progenitor cells 
      from wild type and Ghsr(-/-) mice as well as human umbilical vein endothelial 
      cells in our experiments. We found that ghrelin stimulated endothelial cells 
      angiogenesis and migration through the MEK-ERK signaling pathway. [d-Lys3]-GHRP-6 
      and PD98059 could reverse the effects of ghrelin on endothelial cells. Our study 
      indicates that ghrelin activates its receptor on endothelial cells to promote 
      angiogenesis and migration via a mechanism involving the extracellular regulated 
      protein kinases (ERK) signaling pathway.
FAU - Wang, Jun
AU  - Wang J
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Peking University Health Science Center, Key Laboratory of Molecular 
      Cardiovascular Science, Ministry of Education, Beijing 100191, China. 
      wangjun_901016@sina.com.
FAU - He, Lin
AU  - He L
AD  - Department of Biochemistry and Molecular Biology, School of Basic Medical 
      Sciences, Peking University Health Science Center, Key Laboratory of 
      Carcinogenesis and Translational Research (Ministry of Education), Beijing 
      100191, China. helin910329@126.com.
FAU - Huwatibieke, Bahetiyaer
AU  - Huwatibieke B
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Peking University Health Science Center, Key Laboratory of Molecular 
      Cardiovascular Science, Ministry of Education, Beijing 100191, China. 
      tafcalgen@163.com.
FAU - Liu, Lingchao
AU  - Liu L
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Peking University Health Science Center, Key Laboratory of Molecular 
      Cardiovascular Science, Ministry of Education, Beijing 100191, China. 
      liulingchao@bjmu.edu.cn.
FAU - Lan, He
AU  - Lan H
AD  - Department of Clinical Laboratory, Capital Medical University, Beijing 100053, 
      China. bylanhe08@126.com.
FAU - Zhao, Jing
AU  - Zhao J
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Peking University Health Science Center, Key Laboratory of Molecular 
      Cardiovascular Science, Ministry of Education, Beijing 100191, China. 
      pujingle@163.com.
FAU - Li, Yin
AU  - Li Y
AUID- ORCID: 0000-0002-4019-3391
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Peking University Health Science Center, Key Laboratory of Molecular 
      Cardiovascular Science, Ministry of Education, Beijing 100191, China. 
      yinli@bjmu.edu.cn.
FAU - Zhang, Weizhen
AU  - Zhang W
AUID- ORCID: 0000-0001-8791-2798
AD  - Department of Physiology and Pathophysiology, School of Basic Medical Sciences, 
      Peking University Health Science Center, Key Laboratory of Molecular 
      Cardiovascular Science, Ministry of Education, Beijing 100191, China. 
      weizhenzhang@bjmu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20180826
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Ghrelin)
RN  - 0 (Ghsr1a protein, human)
RN  - 0 (Receptors, Ghrelin)
SB  - IM
MH  - Adipose Tissue/metabolism
MH  - Animals
MH  - Body Weight
MH  - Cell Line, Tumor
MH  - Cell Movement/drug effects
MH  - Disease Models, Animal
MH  - Endothelial Cells/*drug effects/*metabolism
MH  - Ghrelin/*metabolism/pharmacology
MH  - Humans
MH  - *MAP Kinase Signaling System
MH  - Mice
MH  - Mice, Knockout
MH  - *Neovascularization, Physiologic/drug effects
MH  - Phosphorylation
MH  - Receptors, Ghrelin/antagonists & inhibitors/genetics/metabolism
PMC - PMC6164813
OTO - NOTNLM
OT  - ERK
OT  - angiogenesis
OT  - endothelial cells
OT  - ghrelin
OT  - migration
COIS- The authors declare no conflict of interest.
EDAT- 2018/08/29 06:00
MHDA- 2018/12/12 06:00
PMCR- 2018/09/01
CRDT- 2018/08/29 06:00
PHST- 2018/05/18 00:00 [received]
PHST- 2018/08/16 00:00 [revised]
PHST- 2018/08/19 00:00 [accepted]
PHST- 2018/08/29 06:00 [entrez]
PHST- 2018/08/29 06:00 [pubmed]
PHST- 2018/12/12 06:00 [medline]
PHST- 2018/09/01 00:00 [pmc-release]
AID - ijms19092530 [pii]
AID - ijms-19-02530 [pii]
AID - 10.3390/ijms19092530 [doi]
PST - epublish
SO  - Int J Mol Sci. 2018 Aug 26;19(9):2530. doi: 10.3390/ijms19092530.