PMID- 24333598
OWN - NLM
STAT- MEDLINE
DCOM- 20140331
LR  - 20231213
IS  - 1090-2422 (Electronic)
IS  - 0014-4827 (Linking)
VI  - 321
IP  - 2
DP  - 2014 Feb 15
TI  - Endothelial connexin32 enhances angiogenesis by positively regulating tube 
      formation and cell migration.
PG  - 133-41
LID - S0014-4827(13)00519-3 [pii]
LID - 10.1016/j.yexcr.2013.12.002 [doi]
AB  - The gap junction proteins connexin32 (Cx32), Cx37, Cx40, and Cx43 are expressed 
      in endothelial cells, and regulate vascular functions involving inflammation, 
      vasculogenesis and vascular remodeling. Aberrant Cxs expression promotes the 
      development of atherosclerosis which is modulated by angiogenesis; however the 
      role played by endothelial Cxs in angiogenesis remains unclear. In this study, we 
      determined the effects of endothelial Cxs, particularly Cx32, on angiogenesis. 
      EA.hy926 cells that had been transfected to overexpress Cx32 significantly 
      increased capillary length and the number on branches compared to Cx-transfectant 
      cells over-expressing Cx37, Cx40, and Cx43 or mock-treated cells. Treatment via 
      intracellular transfer of anti-Cx32 antibody suppressed tube formation of human 
      umbilical vein endothelial cells (HUVECs) compared to controls. In vitro wound 
      healing assays revealed that Cx32-transfectant cells significantly increased the 
      repaired area while anti-Cx32 antibody-treated HUVECs reduced it. Ex vivo aorta 
      ring assays and in vivo matrigel plaque assays showed that Cx32-deficient mice 
      impaired both vascular sprouting from the aorta and cell migration into the 
      implanted matrigel. Therefore endothelial Cx32 facilitates tube formation, wound 
      healing, vascular sprouting, and cell migration. Our results suggest that 
      endothelial Cx32 positively regulates angiogenesis by enhancing endothelial cell 
      tube formation and cell migration.
CI  - (c) 2013 Published by Elsevier Inc.
FAU - Okamoto, Takayuki
AU  - Okamoto T
AD  - Department of Molecular Pathobiology and Cell Adhesion Biology, Mie University 
      Graduate School of Medicine, 2-174 Edobashi, Tsu-city, Mie 514-8507, Japan.
FAU - Akita, Nobuyuki
AU  - Akita N
AD  - Faculty of Medical Engineering, Suzuka University of Medical Science, 1001-1 
      Kishioka-cho, Suzuka-city, Mie 510-0293, Japan.
FAU - Kawamoto, Eiji
AU  - Kawamoto E
AD  - Department of Molecular Pathobiology and Cell Adhesion Biology, Mie University 
      Graduate School of Medicine, 2-174 Edobashi, Tsu-city, Mie 514-8507, Japan; 
      Emergency and Critical Care Center, Mie University Hospital, 2-174 Edobashi, Tsu 
      514-8507, Japan.
FAU - Hayashi, Tatsuya
AU  - Hayashi T
AD  - Department of Biochemistry, Mie Prefecture College of Nursing, 1-1-1 Yumegaoka, 
      Tsu-city, Mie 514-0116, Japan.
FAU - Suzuki, Koji
AU  - Suzuki K
AD  - Faculty of Pharmaceutical Sciences, Suzuka University of Medical Science, 3500-3 
      Minamitamagaki-cho, Suzuka City 513-8679, Japan.
FAU - Shimaoka, Motomu
AU  - Shimaoka M
AD  - Department of Molecular Pathobiology and Cell Adhesion Biology, Mie University 
      Graduate School of Medicine, 2-174 Edobashi, Tsu-city, Mie 514-8507, Japan. 
      Electronic address: shimaoka@doc.medic.mie-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20131211
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Connexins)
SB  - IM
MH  - Animals
MH  - Capillaries/growth & development/physiology
MH  - Cell Movement/*genetics
MH  - Cells, Cultured
MH  - Connexins/*physiology
MH  - Endothelium, Vascular/*metabolism
MH  - Human Umbilical Vein Endothelial Cells/pathology/physiology
MH  - Humans
MH  - Mice
MH  - Mice, Knockout
MH  - Morphogenesis/genetics
MH  - Neovascularization, Physiologic/*genetics
MH  - Gap Junction beta-1 Protein
OTO - NOTNLM
OT  - Angiogenesis
OT  - Cell migration
OT  - Endothelial cells
OT  - Gap junctions
OT  - Tube formation
EDAT- 2013/12/18 06:00
MHDA- 2014/04/01 06:00
CRDT- 2013/12/17 06:00
PHST- 2013/07/09 00:00 [received]
PHST- 2013/11/29 00:00 [revised]
PHST- 2013/12/02 00:00 [accepted]
PHST- 2013/12/17 06:00 [entrez]
PHST- 2013/12/18 06:00 [pubmed]
PHST- 2014/04/01 06:00 [medline]
AID - S0014-4827(13)00519-3 [pii]
AID - 10.1016/j.yexcr.2013.12.002 [doi]
PST - ppublish
SO  - Exp Cell Res. 2014 Feb 15;321(2):133-41. doi: 10.1016/j.yexcr.2013.12.002. Epub 
      2013 Dec 11.