作者: Sandra K. Masur , Sevastiani Petridou , Paula Folger , Dania Zekaria , Olga Maltseva
DOI:
关键词: Growth factor 、 Fibroblast 、 Cellular differentiation 、 Fibroblast growth factor 、 Stress fiber 、 Blot 、 Biology 、 Molecular biology 、 Myofibroblast 、 Transforming growth factor
摘要: Purpose Keratocytes give rise to fibroblasts and myofibroblasts in wounded cornea. It is well established that treatment of with transforming growth factor (TGF) beta will induce myofibroblast differentiation. We investigated whether this differentiation could be reversed by the administration fibroblast (FGF). Methods Cultured corneal were plated at 200 cells/mm(2), cells grown DMEM/F12 containing (1) 10% FBS or (2) FGF heparin (3) 1% (4) TGF-beta. As distinguished from phenotype, phenotype was identified assembly alpha-smooth muscle (SM) actin protein into stress fiber cytoskeleton. To further characterize regulation two phenotypes, phenotypic expression TGF-beta receptor types I II, cadherins, connexin 43 immunocytochemistry, Western blot analysis, immunoprecipitation alpha-SM mRNA Northern analysis evaluated. Results Corneal replated presence FGF-1 FGF-2 (20 ng/ml) plus (5 microg/ml) medium had decreased protein, receptors, cadherins. Thus, FGF-heparin promoted phenotype. Administration either 20 ng/ml 5 microg/ml alone not effective. Addition enhanced cell surface receptors cultures. Conclusions -2 This finding supports idea are alternative phenotypes rather than terminally differentiated types.