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Ectopic Telomerase Expression in Dupuytren's Disease Myofibroblasts
Author(s) -
Vaughan Melville B.,
Tomasek James J.,
Noon Miriam C.,
Isiaho Armstrong M.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.823.10
Subject(s) - myofibroblast , telomerase , microbiology and biotechnology , transforming growth factor , ectopic expression , transforming growth factor beta , cancer research , phenotype , telomere , biology , telomerase reverse transcriptase , cell culture , pathology , fibrosis , immunology , medicine , genetics , dna , gene
In vitro studies of disease states often require large quantities of cells; however, replicative senescence limits the availability of such resources. Ectopic telomerase expression is known to immortalize cells with little effect on their normal activites. In this study we used telomerase to immortalize fibroblasts derived from Dupuytren's disease, then studied their ability to differentiate into myofibroblasts. Cells were cultured onto coverslips or within stress‐relaxed collagen lattices in the presence or absence of transforming growth factor‐beta1 (TGF‐beta). Samples of both assays were immunostained with an anti‐smooth muscle alpha‐actin antibody to determine the percentage of myofibroblasts; cell contractility was determined using lattices. In all tests, TGF‐beta increased myofibroblast percentage and contractility. This suggests that telomerase has little effect on myofibroblast differentiation. Similar studies elsewhere determined that telomerase inhibits the myofibroblast phenotype, and so our future goals will include comparing parental to immortalized fibroblasts in their ability to differentiate into myofibroblasts. Supported by UCO Office of Research and Grants, and NIH NCRR P2PRR016478.