A characterization of caveolins/caveolae in cardiac and smooth muscle tissues

dc.contributor.authorWoodman, Scott E.
dc.date.accessioned2018-07-12T17:33:13Z
dc.date.available2018-07-12T17:33:13Z
dc.date.issued2004
dc.description.abstractTo better understand the role of caveola/caveolins in electrically responsive cells we examined cardiac muscle and urogenital smooth muscle tissues in mice genetically engineered to be caveolin deficient.;Only Cav-3 is expressed in adult mouse cardiac myocytes. Caveolin-3 knock-out (Cav-3 KO) mouse hearts fail to express the Cav-3 protein and Cav-3 KO cardiac myocytes do not form caveolae. These hearts still express Cav-1 and Cav-2, corresponding to the caveolae formation in cardiac endothelium. Cav-3 KO hearts are hypertrophy and display a reduction in fractional shortening by gated cardiac MRI and transthoracic echocardiography. Histological analysis also show Cav-3 KO hearts to be hypertrophic with an increase in cellular infiltrates. Although the expression and membrane association of dystophin-glycoprotein complex (DGC) proteins remain unchanged, a DGC marker, alpha-sarcoglycan, is excluded from lipid raft/caveolar domains. Mitogen-Activated Protein Kinase activity is increased in Cav-3 KO hearts. These results suggest that Cav-3 generated caveolae in cardiac myocytes play a role in facilitating membrane signaling.;All caveolin family members are expressed in adult mouse urinary bladder. Cav-1 KO mouse urinary bladders fail to express Cav-1, show a near complete loss of Cav-2, with no significant change in Cav-3 expression. Cav-3 KO mouse urinary bladders fail to express Cav-3, but express Cav-1 and Cav-2 in normal amounts. Caveolae formation was only reduced in Cav-1 KO mouse urinary bladders, showing Cav-1 to be the primary caveolae-forming caveolin family member. Cystometric analysis of urinary bladder function within Cav-1 KO mouse urinary bladders show higher basal, threshold, and spontaneous pressure measurements as compared to wild-type controls. Histological analysis reveals urinary bladder smooth muscle cell hypertrophy in the Cav-1 KO mouse. Cav-1 KO bladder strips have a diminished contractile response to the muscarinic agonist carbachol and KCl membrane depolarization. These results suggest that Cav-1 generated caveolae may play an important role in the facilitation of urinary bladder smooth muscle cell contraction.
dc.identifier.citationSource: Dissertation Abstracts International, Volume: 65-09, Section: B, page: 4430.;Advisors: Michael P. Lisanti.
dc.identifier.urihttps://ezproxy.yu.edu/login?url=http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqm&rft_dat=xri:pqdiss:3142192
dc.identifier.urihttps://hdl.handle.net/20.500.12202/726
dc.publisherProQuest Dissertations & Theses
dc.subjectMolecular biology.
dc.subjectAnimal Physiology.
dc.titleA characterization of caveolins/caveolae in cardiac and smooth muscle tissues
dc.typeDissertation

Files