Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Loss of caveolae, vascular dysfunction, and pulmonary defects in caveolin-1 gene-disrupted mice

Official URL:https://doi.org/10.1126/science.1062688
PubMed:View item in PubMed
Creators Name:Drab, M. and Verkade, P. and Elger, M. and Kasper, M. and Lohn, M. and Lauterbach, B. and Menne, J. and Lindschau, C. and Mende, F. and Luft, F.C. and Schedl, A. and Haller, H. and Kurzchalia, T.V.
Journal Title:Science
Journal Abbreviation:Science
Volume:293
Number:5539
Page Range:2449-2452
Date:28 September 2001
Keywords:Albumins, Aorta, Asthenia, Calcium Signaling, Caveolae, Caveolin 1, Caveolins, Cell Division, Cultured Cells, Cholesterol, Endothelium, Vascular Endothelium, Gene Targeting, Lipids, Lung, Membrane Microdomains, Smooth, Vascular Muscle, Nitric Oxide, Pulmonary Alveoli, Pulmonary Fibrosis, Signal Transduction, Animals, Mice
Abstract: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 that lacked caveolae. The absence of this organelle impaired nitric oxide and calcium signaling in the cardiovascular system, causing aberrations in endothelium-dependent relaxation, contractility, and maintenance of myogenic tone. In addition, the lungs of knockout animals displayed thickening of alveolar septa caused by uncontrolled endothelial cell proliferation and fibrosis, resulting in severe physical limitations in caveolin-1-disrupted mice. Thus, caveolin-1 and caveolae play a fundamental role in organizing multiple signaling pathways in the cell.
ISSN:0036-8075
Publisher:American Association for the Advancement of Science (U.S.A.)
Item Type:Article

Repository Staff Only: item control page

Open Access
MDC Library