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Loss of Caveolae, Vascular Dysfunction, and Pulmonary Defects in Caveolin-1 Gene-Disrupted Mice
Marek Drab,12Paul Verkade,1Marlies Elger,3Michael Kasper,4Matthias Lohn,23Birgit Lauterbach,23Jan Menne,3Carsten Lindschau,23Fanny Mende,1Friedrich C. Luft,2Andreas Schedl,5Hermann Haller,3Teymuras V. Kurzchalia1*
Caveolae are plasma membrane invaginations that may play an
important role in numerous cellular processes including transport,signaling, and tumor suppression. By targeted disruption of caveolin-1,the main protein component of caveolae, we generated mice thatlacked
caveolae. The absence of this organelle impaired nitricoxide and
calcium signaling in the cardiovascular system, causingaberrations in
endothelium-dependent relaxation, contractility,and maintenance of
myogenic tone. In addition, the lungs of knockoutanimals displayed
thickening of alveolar septa caused by uncontrolledendothelial cell
proliferation and fibrosis, resulting in severephysical
limitations in caveolin-1-disrupted mice. Thus, caveolin-1and
caveolae play a fundamental role in organizing multiple signalingpathways in the cell.
1 Max Planck Institute for Molecular Cell
Biology and Genetics, Pfotenhauer-Strasse 108, D-01307 Dresden,
Germany.
2 Franz Volhard Clinic and
Max-Delbrück-Center for Molecular Medicine, Humboldt University
Berlin, Wiltberg-Strasse 50, D-13125 Berlin, Germany.
3 Hannover Medical School, Karl-Neuberg-Strasse 1, D-30625 Hannover, Germany.
4 Institute of Anatomy,
Technical University of Dresden, Fetscher-Strasse 74, D-01307 Dresden,
Germany.
5 Max-Delbrück-Center for Molecular
Medicine, Robert-Roessle-Strasse 10, D-13125 Berlin, Germany.
*
To whom correspondence should be addressed. E-mail:
kurzchalia{at}mpi-cbg.de
The editors suggest the following Related Resources on Science sites:
In Science Magazine
PERSPECTIVES
Robert G. Parton (28 September 2001) Science293 (5539), 2404.
[DOI: 10.1126/science.1065677] |Summary »|Full Text »|PDF »
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W.-W. Lin, Y.-C. Lin, T.-Y. Chang, S.-H. Tsai, H.-C. Ho, Y.-T. Chen, and V. C. Yang (2006)
J. Histochem. Cytochem.
54, 897-904
|Abstract »|Full Text »|PDF »
Translocation of endothelial nitric oxide synthase: Another feat of amlodipine, a cardiovascular jack-of-all-trades.
Dynamic Regulation of Caveolin-1 Trafficking in the Germ Line and Embryo of Caenorhabditis elegans.
K. Sato, M. Sato, A. Audhya, K. Oegema, P. Schweinsberg, and B. D. Grant (2006)
Mol. Biol. Cell
17, 3085-3094
|Abstract »|Full Text »|PDF »
Caveolin-1 is required for signaling and membrane targeting of EphB1 receptor tyrosine kinase.
M. M. Vihanto, C. Vindis, V. Djonov, D. P. Cerretti, and U. Huynh-Do (2006)
J. Cell Sci.
119, 2299-2309
|Abstract »|Full Text »|PDF »
Caveolin-1-deficient aortic smooth muscle cells show cell autonomous abnormalities in proliferation, migration, and endothelin-based signal transduction.
G. S. Hassan, T. M. Williams, P. G. Frank, and M. P. Lisanti (2006)
Am J Physiol Heart Circ Physiol
290, H2393-H2401
|Abstract »|Full Text »|PDF »
Genetic ablation of caveolin-1 modifies Ca2+ spark coupling in murine arterial smooth muscle cells.
X. Cheng and J. H. Jaggar (2006)
Am J Physiol Heart Circ Physiol
290, H2309-H2319
|Abstract »|Full Text »|PDF »
Caveolin Plays a Central Role in Endothelial Progenitor Cell Mobilization and Homing in SDF-1-Driven Postischemic Vasculogenesis.
E. Sbaa, J. DeWever, P. Martinive, C. Bouzin, F. Frerart, J.-L. Balligand, C. Dessy, and O. Feron (2006)
Circ. Res.
98, 1219-1227
|Abstract »|Full Text »|PDF »
A. Morani, R. P. A. Barros, O. Imamov, K. Hultenby, A. Arner, M. Warner, and J.-A. Gustafsson (2006)
PNAS
103, 7165-7169
|Abstract »|Full Text »|PDF »
Where is endothelial nitric oxide synthase more critical: plasma membrane or Golgi?.
Z.-G. Jin (2006)
Arterioscler. Thromb. Vasc. Biol.
26, 959-961
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Caveolin-1 controls cell proliferation and cell death by suppressing expression of the inhibitor of apoptosis protein survivin.
V. A. Torres, J. C. Tapia, D. A. Rodriguez, M. Parraga, P. Lisboa, M. Montoya, L. Leyton, and A. F. G. Quest (2006)
J. Cell Sci.
119, 1812-1823
|Abstract »|Full Text »|PDF »
