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Maria Kontaridis Laboratory

Maria Kontaridis, PhD  
Cardiovascular Research Cardiovascular
Division Beth Israel Deaconess Medical Center 3 Blackfan Circle
E/CLS #908 Boston MA 02215
Tel: 617-735-4248
Fax: 617-735-4255
e-mail: mkontari@bidmc.harvard.edu  

Education/Training/Appointments:

Dr. Kontaridis received her undergraduate degrees (B.A. and B.S.) from the University of Florida in Classics and Chemistry, and subsequently, went on to obtain her masters degrees in Pharmacology as well as Biomedical and Biological Sciences from Yale University in 1999 and 2001, respectively. In 2002, she was awarded a Ph.D. from Yale University for work with Dr. Anton Bennett on the role of protein tyrosine phosphatases, especially Shp-2, in cell growth and skeletal muscle differentiation. Dr. Kontaridis' interest in continuing to work on Shp-2 phosphatase led her to accept a postdoctoral position with Dr. Benjamin Neel, at the BIDMC in 2003.

In this context, Dr. Kontaridis has made multiple interesting observations about Shp-2 and its role in cardiac pathophysiology and disease. Her work has garnered extramural support from the American Heart Association, the NIH Pathway to Independence Award (K99/R00), the Milton Foundation and more recently the NHLBI (R01).   Dr. Kontaridis was promoted to Instructor in 2007 and to Assistant Professor of Medicine at Harvard Medical School in 2008.   Dr. Kontaridis is actively involved in the BIDMC/Cardiology division as co-organizer of the departmental seminar series and the annual Cardiology Retreat.   She is also a member of the Cardiology Fellowship Selection Committee, serves as a member of the Committee for the Advancement of Women Faculty in the Department of Medicine at BIDMC, and is Chairman of the Research Safety Committee.   Dr. Kontaridis is also a member of the Harvard Medical School Biomedical and Biological Sciences Faculty Program, where she has a joint appointment in the department of Biological Chemistry and Molecular Pharmacology and with the Leder Human Biology and Translational Medicine Program of Harvard Medical School.   In December of 2010, Dr. Kontaridis was appointed Fellow of the American Heart Association.  

Research Interests:

Understanding the signaling pathways that mediate cardiac developmental processes may reveal important clues into the cellular and molecular pathogenesis of heart disease. Specifically, we want to understand how protein-tyrosine phosphatases (PTPs) relate to cardiac development and disease. Our lab's research efforts focus on developmental biology, in vivo analysis of in mouse systems, including disease models, and cardiac biology and stem cell research using primary cultures. Currently, we are studying mouse models in which we can assess the molecular pathogenesis of the cardiac defects associated with Noonan (NS) and LEOPARD (LS) Syndromes, pediatric disorders both attributed primarily to mutations in Shp2. In addition, we are studying how Shp2 may also be involved in the regulation of the small GTPase RhoA to mediate end-stage heart failure.   Shp2, encoded by the PTPN11 gene, is a key positive regulator in most, if not all, receptor tyrosine kinase (RTK) signaling pathways, acting upstream of Ras in the Erk/MAP kinase cascade.   RhoA is a small GTP binding protein involved in important cellular functions including cell proliferation, migration, and cytoskeletal reorganization.     As both of these proteins have recently been implicated in cardiovascular disease, our lab hopes to answer several interesting questions regarding the effects of Shp2 and/or RhoA in cardiomyocyte development and disease.  

Highlighted Publications:

1-Talita M. Marin, Kimberly Keith, Benjamin Davies, David A. Conner, Prajna Guha, Demetrios Kalaitzidis, Xue Wu , Michael Bauer, Roderick Bronson, Kleber G. Franchini, Benjamin G. Neel and Maria I. Kontaridis.  Rapamycin normalizes hypertrophic cardiomyopathy in a mouse model of LEOPARD Syndrome-associated PTPN11 mutation.  JCI, 2011 Feb 21. pii: 44972. doi: 10.1172/JCI44972. Editorial:  RAS signaling pathway mutations and hypertrophic cardiomyopathy: getting into and out of the thick of it, Gelb, B, Tartaglia M., J Clin Invest. 2011;121(3):844-847. doi:10.1172/JCI46399.

2-Stewart RA, Sanda T, Widlund HR, Zhu S, Swanson KD, Hurley AD, Bentires-Alj M, Fisher DE, Kontaridis MI, Look AT, Neel BG.  Phosphatase-Dependent and -Independent Functions of Shp2 in Neural Crest Cells Underlie LEOPARD Syndrome Pathogenesis.  Dev Cell. 2010 May 18;18(5):750-762.

3-Kontaridis MI, Yang W, Bence KK, Cullen D, Wang B, Bodyak N, Ke Q, Hinek A, Kang PM, Liao R, Neel BG. Deletion of Ptpn11 (Shp2) in cardiomyocytes causes dilated cardiomyopathy via effects on the extracellular signal-regulated kinase/mitogen-activated protein kinase and RhoA signaling pathways. Circulation. 2008;117(11):1423-35. Editorial:  Shp Shape - FAKs about hypertrophy, Martin, KA, Hwa, J.,  Circ Res. 2008 October 10; 103(8): 776-778

4-Kontaridis MI, Swanson KD, David FS, Barford D, Neel BG. PTPN11 (Shp2) mutations in LEOPARD syndrome have dominant negative, not activating, effects. J Biol Chem. 2006;281(10):6785-92. 5-Bentires-Alj, M., Kontaridis, M.I., Neel, B.G. Stops along the RAS pathway in human genetic disease. In: Nat Med. 2006 Mar;12(3):283-285. Nature;2006. p. 283-285.