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Joanne E. Murphy-Ullrich

Joanne E. Murphy-Ullrich, PhD
Professor of Pathology
Cell Developmental and Integrative Biology, and Ophthalmology
University of Alabama at Birmingham
G001A Volker Hall
1720 2ND Avenue South
Birmingham, AL 35294-0019, USA
Email: jmurphy@uabmc.edu

Present Position

  • Professor

Societies

  • American Society for Matrix Biology
  • International Society for Matrix Biology
  • International CCN Society

Awards

  • Established Investigator, American Heart Association (AHA-Genentech Special Awardee in Thrombosis) 1997-2000
  • Secretary/Treasurer American Society for Matrix Biology, 2008-2011, 2012-2013
  • Co-Chair, FASEB Summer Research Conference on Thrombospondins and other Matricellular Proteins, July 2010
  • Chair, FASEB Summer Research Conference on Matricellular Proteins, July 2013
  • Conference Chair, 2016 ASMB Biennial Meeting, St. Petersburg, FL
  • 2003-2006 Director, Cell Adhesion and Matrix Research Center, UAB
  • 2006-2014 Co-director, BioMatrix Engineering and Regenerative Medicine Center, UAB
  • 2015-16 President-elect, American Society for Matrix Biology
  • 2017-18 President, American Society for Matrix Biology

Editorial Board

  • The Journal of Biological Chemistry (1996-2001, 2010-2015, 2016-2021)
  • Calcium Binding Proteins (2006-2009)
  • Associate Editor, Matrix Biology 2013-present
  • Guest Editor 2013-2014, Matrix Biology themed issue on Matricellular Proteins
  • Journal of Cell Communication and Signaling, 2014-present

Research Themes

  • Dr. Murphy-Ullrich has expertise in the extracellular matrix with a focus on extracellular matrix remodeling in disease. She received her BSMT degree from Marquette University and her PhD in Pathology from the University of Wisconsin under the direction of Dr. Terry Oberley. She did post-doctoral training with Dr. Deane Mosher at the University of Wisconsin and with Dr. Magnus Hӧӧk at UAB. She has been a faculty member at UAB since 1988.
    Dr. Murphy-Ullrich has held several leadership positions in the area of extracellular matrix biology. She was Director of the UAB Cell Adhesion and Matrix Research Center and co-Director of the BioMatrix Engineering and Regenerative Medicine Center. She was Secretary/Treasurer of ASMB and she is President of the ASMB and was Chair of the 2016 ASMB Biennial Meeting. She chaired the 2013 FASEB Scientific Conference on Matricellular Proteins in Development, Health, and Disease and guest edited a special issue of Matrix Biology on Matricellular Proteins. She has extensively studied the matricellular protein thrombospondin1 (TSP1).
    Additionally, her lab discovered that TSP1 is a major regulator of latent TGF-β activation and established TSP1’s role in regulating TGF-beta activation in a number of diseases. Her lab identified critical sites in TSP1 that induce TGF-beta activation (KRFK) and sites in latent TGF-beta necessary for latency. Based on this work, she developed tools to probe the involvement of TSP1 in regulation of latent TGF-beta in various disease processes, including diabetic nephropathy and cardiomyopathy and in vascular smooth muscle cells in response to metal ions from endovascular stents. The initial tool was a tetrapeptide (LSKL), which reduced myocardial fibrosis and improved left ventricular function in rats with diabetes and hypertension.
    In recent work, initially funded by the Alabama Drug Discovery Alliance (ADDA), she has teamed with the Drug Discovery unit at Southern Research to identify and develop small molecules based on LSKL. A peptide-like compound based on LSKL reduced myeloma tumor burden, stromal IL-6 levels, and osteolytic disease in pre-clinical models of aggressive systemic human myeloma. A goal of Dr. Murphy-Ullrich’s research program is to identify small molecules based on LSKL and bring them to clinical trials for the treatment of disease.
    Her lab also investigates the role of ER calreticulin (CRT) in augmenting TGF-β signaling through NFAT, linking ER stress and fibrosis. She showed that CRT knockdown attenuates TGF-β signaling in VSMCs and that tissue specific knockdown of CRT in the carotid artery reduces neointima formation and collagen deposition. This work establishes a molecular link between ER stress and fibrosis. High glucose and TGF-β stimulate CRT expression in proximal tubule cells and in the proximal tubules of Akita type I diabetic mice. siRNA knockdown of CRT attenuates the ability of glucose and TGF-beta to stimulate extracellular matrix in human proximal tubule cells. Renal specific knockdown of CRT expression through ultrasound-targeted delivery of cre-recombinase plasmid to diabetic CRT floxed mice with uninephrectomy reduces proteinuria, ECM production, and improves morphology and survival.

Selected Research Publications

  • Schultz-Cherry S., Murphy-Ullrich J.E. (1993)
    Thrombospondin causes activation of latent transforming growth factor-ß secreted by endothelial cells by a novel mechanism.
    J. Cell Biol. 122: 923-932.
  • Crawford S.E., Stellmach V., Murphy-Ullrich, J.E., Ribeiro S.M.F., Lawler, J., Boivin, G.P., Hynes R.O., Bouck, N. (1998)
    Thrombospondin is a major activator of TGF-ß in vivo.
    Cell, 93: 1159-1170.
  • Ribeiro, S.M. and Poczatek,M., Schultz-Cherry S, Villain, M, Murphy-Ullrich J.E. (1999)
    The activation sequence of thrombospondin-1 interacts with the latency-associated peptide to regulate activation of latent TGF-.
    J. Biol. Chem 274: 15386-15394.
  • Young GD, Murphy-Ullrich JE. (2004)
    Molecular interactions that confer latency to transforming growth factor-β.
    J Biol Chem, 279: 38032-38039.
  • Van Duyn Graham L, Sweetwyne MT, Pallero MA, Murphy-Ullrich JE.(2010)
    Intracellular calreticulin regulates multiple steps in fibrillar collagen expression, trafficking, and processing into the extracellular matrix.
    J Biol Chem 5; 285(10):7067-78. (PMC2844156).
  • Lu A, Miao M, Schoeb TR, Agarwal A, Murphy-Ullrich JE. (2011)
    Blockade of TSP1-dependent TGF-beta activation in the Akita model of diabetic nephropathy improves renal function but does not impair wound healing,
    Amer J Pathol. 178: 2573-86, (PMC3124297).
  • Murphy-Ullrich, JE, Sage EH.
    Revisiting the Matricellular Concept.
    Matrix Biol. 2014 37:1-14 (PMC4379989) (Corresponding author)
  • Zimmerman KA, Graham LV, Pallero MA, Murphy-Ullrich (2013)
    Calreticulin regulates Transforming Growth Factor-β stimulated extracellular matrix production.
    J Biol Chem, 288: 14584-14598 (PMC3656311)
  • Zimmerman KA, Xing D, Pallero MA, Lu A, Ikawa M, Black L, Hoyt KL, Kabarowski J, Michalak M, Murphy-Ullrich JE.(2015)
    Calreticulin regulates neointima formation and collagen deposition following carotid artery ligation, Journal of Vascular Research.
    J Vasc. Res 52:306-320 (PMC4816666)
  • Lu A, Pallero MA, Lei W, Hong H, Yang Y, Suto MJ, Murphy-Ullrich JE.
    Inhibition of Transforming Growth Factor-β Activation Diminishes Tumor Progression and Osteolytic Bone Disease in Mouse Models of Multiple Myeloma.
    The American journal of pathology. 2016; 186(3):678-90. (PMC4816696)
  • Owusu BY, Zimmerman KA, Murphy-Ullrich JE.
    The role of the endoplasmic reticulum protein calreticulin in mediating TGF-β-stimulated extracellular matrix production in fibrotic disease.
    J Cell Commun Signal. 2017 Oct 28. doi:10.1007/s12079-017-0426-2. [Epub ahead of print]
  • Murphy-Ullrich JE, Suto MJ.
    Thrombospondin-1 regulation of latent TGF-βactivation: A therapeutic target for fibrotic disease.
    Matrix Biol. 2017 Dec 27. pii: S0945-053X(17)30359-1. doi: 10.1016/j.matbio.2017.12.009. [Epub ahead of print] (Corresponding author)