Loss of Caveolae, Vascular Dysfunction, and Pulmonary Defects in Caveolin-1 Gene-Disrupted Mice (VSports app下载)

@article{Drab2001LossOC,
  title={Loss of Caveolae, Vascular Dysfunction, and Pulmonary Defects in Caveolin-1 Gene-Disrupted Mice},
  author={Marek Drab and Paul Verkade and Marlies Elger and Michael Kasper and Matthias Lohn and Birgit Lauterbach and Jan Menne and Carsten Lindschau and Fanny Mende and Friedrich C. Luft and Andreas Schedl and Hermann Haller and Teymuras Vakhtang Kurzchalia},
  journal={Science},
  year={2001},
  volume={293},
  pages={2449 - 2452},
  url={https://api.semanticscholar.org/CorpusID:34616965}
}
By targeted disruption of caveolin-1, the main protein component of caveolae, mice that lacked Caveolae were generated, causing aberrations in endothelium-dependent relaxation, contractility, and maintenance of myogenic tone and indicating a fundamental role in organizing multiple signaling pathways in the cell.

The biology of caveolae: lessons from caveolin knockout mice and implications for human disease.

The generation of caveolin-null mice has confirmed the essential role of three members of the caveolin family in caveolae biogenesis and in the pathophysiology of diverse tissues.

Defects in caveolin-1 cause dilated cardiomyopathy and pulmonary hypertension in knockout mice

In vivo evidence is provided that cav-1 is essential for the control of systemic NO levels and normal cardiopulmonary function and the loss of Cav-1 leads to a dramatic increase in systemic No levels.

"V体育安卓版" Regulation of Cell Signaling and Function by Endothelial Caveolins: Implications in Disease

How caveolin-1 expressed in endothelial cells regulates endothelial cell signaling and function is focused on, with particular emphasis on relevance to disease, including but not limited to Pulmonary and cardiovascular disorders as well as cancer.

"VSports app下载" siRNA-induced caveolin-1 knockdown in mice increases lung vascular permeability via the junctional pathway

Small interfering RNA is used to knock-down caveolin-1 expression in mouse lung endothelia in vivo and shows the concomitant disappearance of caveolae in lung vessel endothelium and dilated inter-endothelial junctions as well as increased lung vascular permeability to albumin via IEJs.

Loss of Caveolin-1 and caveolae leads to increased cardiac cell stiffness and functional decline of the adult zebrafish heart

It is found that cardiac function was impaired in adult cav1-KO fish, which showed a significantly decreased ejection fraction and heart rate and a loss of cardiac elasticity, which might explain the decreased cardiac contraction and function.

Pathophysiological Role of Caveolae in Hypertension

Current knowledge on caveolae in vasculature is described, with special focus on their pathophysiological role in hypertension.

V体育ios版 - Loss of caveolin and heme oxygenase expression in severe pulmonary hypertension.

While caveolin is expressed in lung endothelial, smooth-muscle, and alveolar septal cells, its expression is absent or decreased in plexiform lesions and in some muscularized precapillary arterioles.

Morphologic Analysis of Multiple Tissues in Caveolin-1 Null Mice

The heart, liver, kidney, stomach, pancreas, skin and white adipose of Caveolin-1 null mice showed remarkable reduction in tissue cell size, cytoplasmic reduction, and increased intercellular spaces without a reduction in cell number, speculation that Caveolin1 plays an important role in systemic lipid homeostasis in vivo.

"VSports手机版" Caveolins and heart diseases.

Altered levels of caveolins and related downstream signaling molecules in cardiomyopathies validate the integral participation of caveolin in normal cardiac physiology and have the potential to lead to the manipulation of Caveolins as novel therapeutic targets.

The role of caveolin-1 in pulmonary matrix remodeling and mechanical properties.

P perturbation of cav1 function may contribute to several pulmonary pathologies as the result of the important role played by cav1, as part of the TGF-beta signaling pathway, in the regulation of the pulmonary ECM.
...

VSports - De novo formation of caveolae in lymphocytes by expression of VIP21-caveolin.

The results show that VIP21-caveolin is a key structural component required for caveolar biogenesis and appears homogeneous in size and morphologically indistinguishable from caveolae of nonlymphoid cells.

The caveolae membrane system.

Caveolae constitute an entire membrane system with multiple functions essential for the cell and are capable of importing molecules and delivering them to specific locations within the cell, exporting molecules to extracellular space, and compartmentalizing a variety of signaling activities.

Role of GTP Hydrolysis in Fission of Caveolae Directly from Plasma Membranes

A cell-free system that reconstituted fission of caveolae from lung endothelial plasma membranes was developed using addition of cytosol and the hydrolysis of guanosine triphosphate (GTP) induced caveolar fission.

A Role for Caveolin in Transport of Cholesterol from Endoplasmic Reticulum to Plasma Membrane*

Evidence caveolin is involved in transporting newly synthesized cholesterol from the ER directly to caveolae is presented and cholesterol transport to the cell surface was nearly 4 times more rapid in cells expressing caveolin than in matched cells lacking caveolin.

Differentiation of Vascular Smooth Muscle Cells and the Regulation of Protein Kinase C-α

The activity and immunoreactivity of PKC-α in primary cultures of VSMCs from rat aortas under different conditions of growth and differentiation and in vitro substrate phosphorylation were studied.

How cells handle cholesterol.

The regulation of cholesterol homeostasis is now receiving a new focus, and this changed perspective may throw light on diseases caused by cholesterol excess, the prime example being atherosclerosis.

A Pore-forming Toxin Interacts with a GPI-anchored Protein and Causes Vacuolation of the Endoplasmic Reticulum (VSports注册入口)

The data indicate that binding of proaerolysin to GPI-anchored proteins and processing of the toxin lead to oligomerization and channel formation in the plasma membrane, which in turn causes selective disorganization of early biosynthetic membrane dynamics.

Lipid Domain Structure of the Plasma Membrane Revealed by Patching of Membrane Components

The data strongly suggest that coalescence of cross-linked raft elements is mediated by their common lipid environments, whereas separation of raft and non-raft patches is caused by the immiscibility of different lipid phases, supported by the finding that cholesterol depletion abrogated segregation.

Src tyrosine kinases, Galpha subunits, and H-Ras share a common membrane-anchored scaffolding protein, caveolin. Caveolin binding negatively regulates the auto-activation of Src tyrosine kinases.

It appears that caveolin structurally and functionally interacts with wild-type c-Src via caveolin residues 82-101, and this cytosolic caveolin domain has the following unique features: it is membrane-proximal, suggesting that it may be involved in other potential protein-protein interactions.