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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
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RhoA activation and interaction with Caveolin-1 are critical for pressure-induced myogenic tone in rat mesenteric resistance arteries.
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A New Paradigm: Calcium Independent and Caveolae Internalization Dependent Release of Nitric Oxide by the Endothelial Nitric Oxide Synthase.
G. Bkaily, P. D'Orleans-Juste, and D. Jacques (2006)
Circ. Res.
99, 793-794
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Novel Mechanism of Endothelial Nitric Oxide Synthase Activation Mediated by Caveolae Internalization in Endothelial Cells.
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Circ. Res.
99, 870-877
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Transient anchorage of cross-linked glycosyl-phosphatidylinositol-anchored proteins depends on cholesterol, Src family kinases, caveolin, and phosphoinositides.
Y. Chen, W. R. Thelin, B. Yang, S. L. Milgram, and K. Jacobson (2006)
J. Cell Biol.
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Caveolin-1 Regulates Store-Operated Ca2+ Influx by Binding of Its Scaffolding Domain to Transient Receptor Potential Channel-1 in Endothelial Cells.
A. M. Kwiatek, R. D. Minshall, D. R. Cool, R. A. Skidgel, A. B. Malik, and C. Tiruppathi (2006)
Mol. Pharmacol.
70, 1174-1183
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Transient Receptor Potential Channels and Caveolin-1: Good Friends in Tight Spaces.
A Functional Interaction between Sprouty Proteins and Caveolin-1.
M. A. Cabrita, F. Jaggi, S. P. Widjaja, and G. Christofori (2006)
J. Biol. Chem.
281, 29201-2912
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Caveolin-1 is essential for liver regeneration..
M. A. Fernandez, C. Albor, M. Ingelmo-Torres, S. J. Nixon, C. Ferguson, T. Kurzchalia, F. Tebar, C. Enrich, R. G. Parton, and A. Pol (2006)
Science
313, 1628-1632
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Transvascular protein transport in mice lacking endothelial caveolae.
B.-I. Rosengren, A. Rippe, C. Rippe, D. Venturoli, K. Sward, and B. Rippe (2006)
Am J Physiol Heart Circ Physiol
291, H1371-H1377
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