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Tetraspanin CD151 maintains vascular stability by balancing the forces of cell adhesion and cytoskeletal tension
- Source :
- Blood. 118:4274-4284
- Publication Year :
- 2011
- Publisher :
- American Society of Hematology, 2011.
-
Abstract
- Tetraspanin CD151 is highly expressed in endothelial cells and regulates pathologic angiogenesis. However, the mechanism by which CD151 promotes vascular morphogenesis and whether CD151 engages other vascular functions are unclear. Here we report that CD151 is required for maintaining endothelial capillary-like structures formed in vitro and the integrity of endothelial cell-cell and cell-matrix contacts in vivo. In addition, vascular permeability is markedly enhanced in the absence of CD151. As a global regulator of endothelial cell-cell and cell-matrix adhesions, CD151 is needed for the optimal functions of various cell adhesion proteins. The loss of CD151 elevates actin cytoskeletal traction by up-regulating RhoA signaling and diminishes actin cortical meshwork by down-regulating Rac1 activity. The inhibition of RhoA or activation of cAMP signaling stabilizes CD151-silenced or -null endothelial structure in vascular morphogenesis. Together, our data demonstrate that CD151 maintains vascular stability by promoting endothelial cell adhesions, especially cell-cell adhesion, and confining cytoskeletal tension.
- Subjects :
- rac1 GTP-Binding Protein
rho GTP-Binding Proteins
RHOA
Immunology
Vascular permeability
Cell Communication
Tetraspanin 24
Biology
Biochemistry
Mice
Cell-matrix adhesion
Vascular Biology
Cell Adhesion
Animals
Humans
Cytoskeleton
Cell adhesion
Cells, Cultured
Neuropeptides
Endothelial Cells
Cell Biology
Hematology
Actins
Mice, Mutant Strains
Extracellular Matrix
rac GTP-Binding Proteins
Cell biology
Endothelial stem cell
Rac GTP-Binding Proteins
Vascular endothelial growth factor A
Gene Expression Regulation
biology.protein
Blood Vessels
rhoA GTP-Binding Protein
Subjects
Details
- ISSN :
- 15280020 and 00064971
- Volume :
- 118
- Database :
- OpenAIRE
- Journal :
- Blood
- Accession number :
- edsair.doi.dedup.....fe0e839be7180de25de286d79bf5c04c
- Full Text :
- https://doi.org/10.1182/blood-2011-03-339531