PMID- 18030489
OWN - NLM
STAT- MEDLINE
DCOM- 20080908
LR  - 20211020
IS  - 0948-6143 (Print)
IS  - 0948-6143 (Linking)
VI  - 129
IP  - 2
DP  - 2008 Feb
TI  - Differential role of Rho GTPases in endothelial barrier regulation dependent on 
      endothelial cell origin.
PG  - 179-91
AB  - From studies using macrovascular endothelium, it was concluded that Rho A 
      activation generally leads to endothelial barrier breakdown. Here, we 
      characterized the role of Rho GTPases in endothelial barrier regulation in four 
      different cell lines, both microvascular and macrovascular. Rho A activation by 
      cytotoxic necrotizing factor y (CNFy) induced stress fiber formation in all cell 
      lines. This was paralleled by gap formation and barrier breakdown in 
      microvascular mesenteric endothelial cells (MesEnd), human dermal microvascular 
      endothelial cells (HDMEC) as well as in macrovascular pulmonary artery 
      endothelial cells (PAEC) but not in microvascular myocardial endothelial cells 
      (MyEnd). In MyEnd cells, activation of Rac 1 and Cdc42 by CNF-1 strengthened 
      barrier properties whereas in MesEnd, HDMEC and PAEC all three GTPases were 
      activated which increased permeability in PAEC but not in MesEnd and HDMEC. In 
      PAEC, CNF-1-induced decrease of barrier properties was blocked by the Rho kinase 
      inhibitor Y27632 indicating that co-activation of Rho A dominated the barrier 
      response. Inactivation of Rac 1 by toxin B or by lethal toxin (LT) compromised 
      barrier properties in all cell lines. Taken together, Rac 1 requirement for 
      endothelial barrier maintenance but not the destabilizing role of Rho A seems to 
      be ubiquitous.
FAU - Baumer, Y
AU  - Baumer Y
AD  - Institute of Anatomy and Cell Biology, University of Wurzburg, Koellikerstr. 6, 
      97070 Wurzburg, Germany.
FAU - Burger, S
AU  - Burger S
FAU - Curry, F E
AU  - Curry FE
FAU - Golenhofen, N
AU  - Golenhofen N
FAU - Drenckhahn, D
AU  - Drenckhahn D
FAU - Waschke, J
AU  - Waschke J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071121
PL  - Germany
TA  - Histochem Cell Biol
JT  - Histochemistry and cell biology
JID - 9506663
RN  - 0 (Amides)
RN  - 0 (Bacterial Toxins)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Escherichia coli Proteins)
RN  - 0 (Pyridines)
RN  - 106803-33-2 (cytotoxic necrotizing factor type 1)
RN  - 138381-45-0 (Y 27632)
RN  - EC 3.6.5.2 (cdc42 GTP-Binding Protein)
RN  - EC 3.6.5.2 (rac1 GTP-Binding Protein)
RN  - EC 3.6.5.2 (rho GTP-Binding Proteins)
RN  - EC 3.6.5.2 (rhoA GTP-Binding Protein)
SB  - IM
MH  - Amides/pharmacology
MH  - Animals
MH  - Bacterial Toxins/pharmacology
MH  - Capillary Permeability/drug effects/*physiology
MH  - Cell Line
MH  - Cells, Cultured
MH  - Endothelial Cells/drug effects/*physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Escherichia coli Proteins/pharmacology
MH  - Humans
MH  - Mice
MH  - Pyridines/pharmacology
MH  - Swine
MH  - cdc42 GTP-Binding Protein/physiology
MH  - rac1 GTP-Binding Protein/drug effects/physiology
MH  - rho GTP-Binding Proteins/drug effects/*physiology
MH  - rhoA GTP-Binding Protein/antagonists & inhibitors/*physiology
EDAT- 2007/11/22 09:00
MHDA- 2008/09/09 09:00
CRDT- 2007/11/22 09:00
PHST- 2007/11/01 00:00 [accepted]
PHST- 2007/11/22 09:00 [pubmed]
PHST- 2008/09/09 09:00 [medline]
PHST- 2007/11/22 09:00 [entrez]
AID - 10.1007/s00418-007-0358-7 [doi]
PST - ppublish
SO  - Histochem Cell Biol. 2008 Feb;129(2):179-91. doi: 10.1007/s00418-007-0358-7. Epub 
      2007 Nov 21.