Abstract
The cavins are a family of proteins associated with caveolae, cavin-1, -2 and -3 being widely expressed while cavin-4 is restricted to striated muscle. Deletion of cavin-1 results in phenotypes including metabolic changes consistent with adipocyte dysfunction, and caveolae are completely absent. Deletion of cavin-2 causes tissue-specific loss of caveolae. The consequences of cavin-3 deletion are less clear, as there are divergent data on the abundance of caveolae in cavin-3 null mice. Here we examine the consequences of cavin-3 deficiency in vivo by making cavin-3 knockout mice. We find that loss of cavin-3 has minimal or no effects on the levels of other caveolar proteins, does not appear to play a major role in formation of protein complexes important for caveolar morphogenesis, and has no significant effect on caveolae abundance. Cavin-3 null mice have the same body weight and fat mass as wild type animals at ages 8 through 30 weeks on both normal chow and high fat diets. Likewise, the two mouse strains exhibit identical glucose tolerance tests on both diets. Microarray analysis from adipose tissue shows that the changes in mRNA expression between cavin-3 null and wild type mouse are minimal. We conclude that cavin-3 is not absolutely required for making caveolae, and suggest that the mechanistic link between cavin-3 and metabolic regulation remains uncertain.
Highlights
Caveolae were first defined by their appearance as ‘‘little caves’’ that were observed in electron micrographs of cell surfaces [1,2]
Cavin-3 does not play a major role on caveolae formation Cavin-3 knockout mice were generated independently
Likewise there is no major impact of cavin-3 deficiency on caveolae formation (Fig. 2A, [19]), or the assembly of caveolar proteins into high molecular weight complexes (Fig. 2B, [19])
Summary
Caveolae were first defined by their appearance as ‘‘little caves’’ that were observed in electron micrographs of cell surfaces [1,2]. Caveolae have been suggested to play a role in a variety of pathologies, including cancer, diabetes, and cardiovascular disease and loss of caveolae causes muscular and lipodystrophies, insulin resistance and cardiovascular defects amongst a variety of other abnormalities (reviewed in [5]) It has been suggested caveolae plays a role as mechanosensor [6]. Cavin-2 deficiency in mice causes a tissue-specific loss of caveolae affecting lung and adipose endothelium, but not the endothelium of skeletal and cardiac muscle [19]. Cavin-3 deficiency in mice as reported by Hansen et al was without apparent effect on caveolae abundance in the endothelium of lung, heart, skeletal muscle and adipose tissue, and in the adipocytes of abdominal fat [19]. We observe minimal changes in caveolae number and in the level of cavin-1, and no apparent metabolic changes in mice on normal and high fat diets at 30 weeks of age
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