Show simple item record

dc.contributor.authorWoodman, Scott E.
dc.date.accessioned2018-07-12T17:33:13Z
dc.date.available2018-07-12T17:33:13Z
dc.date.issued2004
dc.identifier.citationSource: Dissertation Abstracts International, Volume: 65-09, Section: B, page: 4430.;Advisors: Michael P. Lisanti.
dc.identifier.urihttps://yulib002.mc.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.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.publisherProQuest Dissertations & Theses
dc.subjectMolecular biology.
dc.subjectAnimal Physiology.
dc.titleA characterization of caveolins/caveolae in cardiac and smooth muscle tissues
dc.typeDissertation


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

Show simple item record