Phillip Michael Bauer

Publications (2)18.63 Total impact

• Source

  Available from: William C Sessa

  Article: Reexpression of caveolin-1 in endothelium rescues the vascular, cardiac, and pulmonary defects in global caveolin-1 knockout mice.

  Takahisa Murata, Michelle I Lin, Yan Huang, Jun Yu, Phillip Michael Bauer, Frank J Giordano, William C Sessa
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  ABSTRACT: Caveolin-1 (Cav-1) is the principal structural component of caveolae organelles in smooth muscle cells, adipocytes, fibroblasts, epithelial cells, and endothelial cells (ECs). Cav-1-deficient (Cav-1 knockout [KO]) mice are viable and show increases of nitric oxide (NO) production in vasculature, cardiomyopathy, and pulmonary dysfunction. In this study, we generated EC-specific Cav-1-reconstituted (Cav-1 RC) mice and reexamined vascular, cardiac, and pulmonary phenotypes. Cav-1 KO pulmonary arteries had decreased smooth muscle contractility and increased endothelial NO synthase activation and hypotension; the latter two effects were rescued completely in Cav-1 RC mice. Cav-1 KO mice exhibited myocardial hypertrophy, pulmonary hypertension, and alveolar cell hyperproliferation caused by constitutive activation of p42/44 mitogen-activated protein kinase and Akt. Interestingly, in Cav-1 RC mice, cardiac hypertrophy and pulmonary hypertension were completely rescued, whereas alveolar hyperplasia was partially recovered because of the lack of rescue of Cav-1 in bronchiolar epithelial cells. These results provide clear physiological evidence supporting the important role of cell type-specific Cav-1 expression governing multiple phenotypes in the vasculature, heart, and lung.
  Journal of Experimental Medicine 11/2007; 204(10):2373-82. · 13.85 Impact Factor
• Article: Genetic evidence supporting caveolae microdomain regulation of calcium entry in endothelial cells.

  Takahisa Murata, Michelle I Lin, Radu V Stan, Phillip Michael Bauer, Jun Yu, William C Sessa
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  ABSTRACT: Various cellular signals initiate calcium entry into cells, and there is evidence that lipid rafts and caveolae may concentrate proteins that regulate transmembrane calcium fluxes. Here, using mice deficient in caveolin-1 (Cav-1) and Cav-1 knock-out reconstituted with endothelium-specific Cav-1, we show that Cav-1 is essential for calcium entry in endothelial cells and governs the localization and protein-protein interactions between transient receptor channels C4 and C1. Thus, Cav-1 is required for calcium entry in vascular endothelial cells and perhaps other specialized cell types containing caveolae.
  Journal of Biological Chemistry 07/2007; 282(22):16631-43. · 4.77 Impact Factor