M‐caveolin, a muscle‐specific caveolin‐related protein

Way, Michael; Parton, Robert G.

doi:10.1016/0014-5793(95)01256-7

Cited by 215 publications

(167 citation statements)

References 37 publications

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“…However, a molecular understanding of cardiac myocyte caveolae only began recently in the mid 1990s with the identification of Cav-3, a muscle-specific caveolin-related protein (2,4,6). Since the molecular identification and cloning of Cav-3, a wealth of in vitro data has accumulated demonstrating a role for Cav-3 in cardiac myocyte signaling (19 -27).…”

Section: Discussionmentioning

confidence: 99%

Caveolin-3 Knock-out Mice Develop a Progressive Cardiomyopathy and Show Hyperactivation of the p42/44 MAPK Cascade

Woodman

Park

Cohen

et al. 2002

Journal of Biological Chemistry

265

241

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A growing body of evidence suggests that muscle cell caveolae may function as specialized membrane microdomains in which the dystrophin-glycoprotein complex and cellular signaling molecules reside. Caveolin-3 (Cav-3) is the only caveolin family member expressed in striated muscle cell types (cardiac and skeletal). Interestingly, skeletal muscle fibers from Cav-3 (؊/؊) knockout mice show a number of myopathic changes, consistent with a mild-to-moderate muscular dystrophy phenotype. However, it remains unknown whether a loss of Cav-3 affects the phenotypic behavior cardiac myocytes in vivo. Here, we present a detailed characterization of the hearts of Cav-3 knock-out mice. We show that these mice develop a progressive cardiomyopathic phenotype. At four months of age, Cav-3 knock-out hearts display significant hypertrophy, dilation, and reduced fractional shortening, as revealed by gated cardiac MRI and transthoracic echocardiography. Histological analysis reveals marked cardiac myocyte hypertrophy, with accompanying cellular infiltrates and progressive interstitial/peri-vascular fibrosis. Interestingly, loss of Cav-3 expression in the heart does not change the expression or the membrane association of the dystrophin-glycoprotein (DG) complex. However, a marker of the DG complex, ␣-sarcoglycan, was specifically excluded from lipid raft domains in the absence of Cav-3. Because activation of the Ras-p42/44 MAPK pathway in cardiac myocytes can drive cardiac hypertrophy, we next assessed the activation state of this pathway using a phospho-specific antibody probe. We show that p42/44 MAPK (ERK1/2) is hyperactivated in hearts derived from Cav-3 knock-out mice. These results are consistent with previous in vitro data demonstrating that caveolins may function as negative regulators of the p42/44 MAPK cascade. Taken together, our data argue that loss of Cav-3 expression is sufficient to induce a molecular program leading to cardiac myocyte hypertrophy and cardiomyopathy.

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Section: Discussionmentioning

confidence: 99%

Caveolin-3 Knock-out Mice Develop a Progressive Cardiomyopathy and Show Hyperactivation of the p42/44 MAPK Cascade

Woodman

Park

Cohen

et al. 2002

Journal of Biological Chemistry

265

241

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“…In comparison, knockout of either CAV1 or CAV3 results in a loss of caveolae formations in the specific cell type for which they are expressed [35,36]. Notably, it was originally believed that expression of CAV3 was restricted to skeletal and smooth muscle cells [26,[37][38][39]. We now know this not to be the case, as expression of CAV3 is more widespread, including its presence in nervous tissue [30].…”

Section: Caveolins: Important For the Trafficking And Clustering Of Mmentioning

confidence: 99%

Caveolin proteins and estrogen signaling in the brain

Luoma

Boulware

Mermelstein

2008

Molecular and Cellular Endocrinology

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Best described outside the nervous system, caveolins are structural proteins that form caveolae, functional microdomains at the plasma membrane that cluster related signaling molecules. Caveolin associated proteins include G protein coupled receptors and G proteins, receptor tyrosine kinases, as well as protein kinases, ion channels and various other signaling enzymes. Not surprisingly, a wide array of biological disorders are thought to be rooted in caveolin dysfunction. In addition, caveolins also traffic and cluster estrogen receptors to caveolae. Interactions between the estrogen receptors ERα and ERβ with caveolins appear critical in many non-neuronal cell types, e.g. disruption of normal function may underlie many forms of breast cancer. Recent findings suggest caveolins may also play an essential role in membrane estrogen receptor function in the nervous system. Not only are they expressed in neurons and glia, but different caveolin isoforms also appear necessary to generate distinct functional signaling complexes. With membrane estrogen receptors responsible for the efficient activation of a multitude of intracellular signaling pathways, which in turn influence a wide variety of nervous system functions, caveolin proteins are poised to act as the central coordinators of these processes.

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“…Recently two homologues of the protein have been identified [29][30][31], with one of these homologues being expressed exclusively in muscle [29,31]. In this review for the sake of simplicity, caveolin-1 will be used instead of VIP21-caveolin (see [41]).…”

Section: Caveolae and Vip21-caveolinmentioning

confidence: 99%

And still they are moving… Dynamic properties of caveolae

Kurzchalia

Parton

1996

FEBS Letters

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Caveolae are structures found on the surface of many mammalian cells. In the last few years the biogenesis and the function of these organelles have been intensively investigated but many challenging questions remain. One of these is whether caveolae are statically attached to the cytoplasmic surface of the plasma membrane or are moving to other intracellular organelles. Also the cycling of the caveolar coat component, VIP21-caveolin, is a subject of intensive discussion. The solution to these problems could give an insight into the understanding of caveolar function.

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M‐caveolin, a muscle‐specific caveolin‐related protein

Cited by 215 publications

References 37 publications

Caveolin-3 Knock-out Mice Develop a Progressive Cardiomyopathy and Show Hyperactivation of the p42/44 MAPK Cascade

Caveolin-3 Knock-out Mice Develop a Progressive Cardiomyopathy and Show Hyperactivation of the p42/44 MAPK Cascade

Caveolin proteins and estrogen signaling in the brain

And still they are moving… Dynamic properties of caveolae

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