PMID- 12225983
OWN - NLM
STAT- MEDLINE
DCOM- 20021008
LR  - 20200930
IS  - 0363-6143 (Print)
IS  - 0363-6143 (Linking)
VI  - 283
IP  - 4
DP  - 2002 Oct
TI  - Role of alpha(v)beta(3)-integrin in TNF-alpha-induced endothelial cell migration.
PG  - C1196-205
AB  - Tumor necrosis factor-alpha (TNF-alpha), one of the major inflammatory cytokines, 
      is known to influence endothelial cell migration. In this study, we demonstrate 
      that exposure of calf pulmonary artery endothelial cells to TNF-alpha caused an 
      increase in the formation of membrane protrusions and cell migration. 
      Fluorescence microscopy revealed an increase in alpha(v)beta(3) focal contacts 
      but a decrease in alpha(5)beta(1) focal contacts in TNF-alpha-treated cells. In 
      addition, both cell-surface and total cellular expression of 
      alpha(v)beta(3)-integrins increased significantly, whereas the expression of 
      alpha(5)beta(1)-integrins was unaltered. Only focal contacts containing 
      alpha(v)beta(3)- but not alpha(5)beta(1)-integrins were present in membrane 
      protrusions of cells at the migration front. In contrast, robust focal contacts 
      containing alpha(5)beta(1)-integrins were present in cells behind the migration 
      front. A blocking antibody to alpha(v)beta(3), but not a blocking antibody to 
      alpha(5)-integrins, significantly inhibited TNF-alpha-induced cell migration. 
      These results indicate that in response to TNF-alpha, endothelial cells may 
      increase the activation and ligation of alpha(v)beta(3) while decreasing the 
      activation and ligation of alpha(5)beta(1)-integrins to facilitate cell 
      migration, a process essential for vascular wound healing and angiogenesis.
FAU - Gao, Baochong
AU  - Gao B
AD  - Department of Physiology, Albany Medical College, Albany, NY 12208, USA. 
      baochong.gao@med.va.gov
FAU - Saba, Thomas M
AU  - Saba TM
FAU - Tsan, Min-Fu
AU  - Tsan MF
LA  - eng
GR  - GM 21447/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol Cell Physiol
JT  - American journal of physiology. Cell physiology
JID - 100901225
RN  - 0 (Antibodies, Blocking)
RN  - 0 (Receptors, Fibronectin)
RN  - 0 (Receptors, Vitronectin)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antibodies, Blocking/pharmacology
MH  - Cattle
MH  - Cell Adhesion/drug effects
MH  - Cell Line
MH  - Cell Movement/*drug effects
MH  - Cell Surface Extensions/drug effects/physiology
MH  - Dose-Response Relationship, Drug
MH  - Endothelium, Vascular/cytology/*drug effects/*metabolism
MH  - Focal Adhesions/drug effects/metabolism/ultrastructure
MH  - Microscopy, Fluorescence
MH  - Pulmonary Artery
MH  - Receptors, Fibronectin/antagonists & inhibitors/metabolism
MH  - Receptors, Vitronectin/antagonists & inhibitors/*metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 2002/09/13 10:00
MHDA- 2002/10/09 04:00
CRDT- 2002/09/13 10:00
PHST- 2002/09/13 10:00 [pubmed]
PHST- 2002/10/09 04:00 [medline]
PHST- 2002/09/13 10:00 [entrez]
AID - 10.1152/ajpcell.00064.2002 [doi]
PST - ppublish
SO  - Am J Physiol Cell Physiol. 2002 Oct;283(4):C1196-205. doi: 
      10.1152/ajpcell.00064.2002.