Key result
Cavin-1 deficient mice exhibited vascular remodeling, increased pulmonary blood pressure, right ventricular hypertrophy, and altered expression of Arg1 and Ddah1.
Cavin-1 deficiency in mice leads to pulmonary vascular remodeling and pulmonary hypertension, associated with altered Arg1 and Ddah1 expression.
Cavin-1 deficiency induces pulmonary hypertension in mice; leaves open relevance to human disease and therapeutic targeting.
Caveolae are invaginations in the plasma membrane that depend on caveolins and cavins for maturation. Here, we investigated the pulmonary phenotype in mice lacking cavin-1. Bright field and electron-microscopy showed that the cavin-1-deficient mice lacked caveolae in the lung, had an increased lung tissue density, and exhibited hypertrophic remodeling of pulmonary arteries. The right ventricle of the heart moreover had an increased mass and the right ventricular pressure was elevated. A microarray analysis revealed upregulation of Arg1 and downregulation of Ddah1, molecules whose altered expression has previously been associated with pulmonary arterial hypertension. Taken together, this work demonstrates vascular remodeling and increased pulmonary blood pressure in cavin-1 deficient mice and associates this phenotype with altered expression of Arg1 and Ddah1.
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Swärd et al. (2013) studied Pulmonary arterial hypertension phenotype. Cavin-1 deficiency was evaluated on Pulmonary phenotype including lung tissue density, vascular remodeling, right ventricular pressure, and gene expression. Cavin-1 deficient mice exhibited vascular remodeling, increased pulmonary blood pressure, right ventricular hypertrophy, and altered expression of Arg1 and Ddah1.
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