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INDIVIDUAL RESEARCHER

Livingston Van De Water , Ph.D.
Professor
e-mail: vandewl@mail.amc.edu


Education

1979 - Ph.D. from University of Rochester


Current Research

Myofibroblasts are prominent and persistent components within the tumor microenvironment where they support both carcinoma progression and tumor angiogenesis. During normal, acute wound healing, myofibroblasts assemble a scar that has minimal impact on tissue function. However, during fibrosis, a form of pathogenic healing, myofibroblasts deposit functionally inappropriate amounts of scar in organs such as skin, lung, liver and kidney. Our research is focused on understanding the cellular and molecular mechanisms that control the conversion of fibroblasts to myofibroblasts and regulate myofibroblast persistence in pathogenic settings, such as tumor stroma and organ fibrosis. To do so, we are testing how growth factors, extracellular matrix proteins, such as fibronectin, integrins and focal adhesion proteins work coordinately to regulate myofibroblast persistence and function. Our overall goal is to develop a basis for novel therapeutics that will modulate myofibroblast generation, function and persistence in pathogenic tissue repair and tumor stroma.




References

  1. Meckmongkol TT, Harmon R, McKeown-Longo P, Van De Water L: The fibronectin synergy site modulates TGF-ß-dependent fibroblast contraction. Biochem Biophys Res Commun 360:709-714, 2007.


  2. Dabiri G, Tumbarello DA, Turner CE, Van De Water L: TGF-²1 slows the growth of pathogenic myofibroblasts through a mechanism requiring the focal adhesion protein, Hic-5. J Invest Dermatol 128:280-291, 2008.


  3. Shinde AV, Bystroff C, Wang C, Vogelzang, MG, Vincent PA, Hynes RO, Van De Water L: Identification of the peptide sequences within the EIIIA (ED-A) segment that mediate integrin a9ß1-dependent cellular activities. J Biol Chem 283:2858-2870, 2008.


  4. Dabiri T, Tumbarello DA, Turnder CE, Van De Water L: Hic-5 promtes the hypertrophic scar myofibroblast phenotype by regulating the TGF-ß1 autocrine loop. J Invest Dermatol 128:2518-2525, 2008.


  5. Singh P, Chen C, Stepp MA, Sheppard D, Van De Water L: Loss of integrin a9/ß1 results in defects in proliferation, causing poor re-epithelialization during cutaneous wound healing. J Invest Dermatol 129:217-228, 2009.