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Medicine and Health Sciences Commons

Open Access. Powered by Scholars. Published by Universities.®

Cardiology

Thomas Jefferson University

Center for Translational Medicine Faculty Papers

Series

Hypertrophy

Publication Year

Articles 1 - 2 of 2

Full-Text Articles in Medicine and Health Sciences

Gsk-3alpha Directly Regulates Beta-Adrenergic Signaling And The Response Of The Heart To Hemodynamic Stress In Mice., Jibin Zhou, Hind Lal, Xiongwen Chen, Xiying Shang, Jianliang Song, Yingxin Li, Risto Kerkela, Bradley W Doble, Katrina Macaulay, Morgan Decaul, Walter J Koch, John Farber, James Woodgett, Erhe Gao, Thomas Force Jul 2010

Gsk-3alpha Directly Regulates Beta-Adrenergic Signaling And The Response Of The Heart To Hemodynamic Stress In Mice., Jibin Zhou, Hind Lal, Xiongwen Chen, Xiying Shang, Jianliang Song, Yingxin Li, Risto Kerkela, Bradley W Doble, Katrina Macaulay, Morgan Decaul, Walter J Koch, John Farber, James Woodgett, Erhe Gao, Thomas Force

Center for Translational Medicine Faculty Papers

The glycogen synthase kinase-3 (GSK-3) family of serine/threonine kinases consists of 2 highly related isoforms, alpha and beta. Although GSK-3beta has an important role in cardiac development, much remains unknown about the function of either GSK-3 isoform in the postnatal heart. Herein, we present what we believe to be the first studies defining the role of GSK-3alpha in the mouse heart using gene targeting. Gsk3a(-/-) mice over 2 months of age developed progressive cardiomyocyte and cardiac hypertrophy and contractile dysfunction. Following thoracic aortic constriction in young mice, we observed enhanced hypertrophy that rapidly transitioned to ventricular dilatation and contractile dysfunction. …


P5l Mutation In Ank Results In An Increase In Extracellular Inorganic Pyrophosphate During Proliferation And Nonmineralizing Hypertrophy In Stably Transduced Atdc5 Cells, Raihana Zaka, David Stokes, Arnold S. Dion, Anna Kusnierz, Fei Han, Charlene J. Williams Oct 2006

P5l Mutation In Ank Results In An Increase In Extracellular Inorganic Pyrophosphate During Proliferation And Nonmineralizing Hypertrophy In Stably Transduced Atdc5 Cells, Raihana Zaka, David Stokes, Arnold S. Dion, Anna Kusnierz, Fei Han, Charlene J. Williams

Center for Translational Medicine Faculty Papers

Ank is a multipass transmembrane protein that regulates the cellular transport of inorganic pyrophosphate. In the progressive ankylosis (ank) mouse, a premature termination mutation at glutamic acid 440 results in a phenotype characterized by inappropriate deposition of basic calcium phosphate crystals in skeletal tissues. Mutations in the amino terminus of ANKH, the human homolog of Ank, result in familial calcium pyrophosphate dihydrate deposition disease. It has been hypothesized that these mutations result in a gain-of-function with respect to the elaboration of extracellular inorganic pyrophosphate. To explore this issue in a mineralization-competent system, we stably transduced ATDC5 cells with wild-type Ank …