FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence
Autoři | |
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Rok publikování | 2010 |
Druh | Článek v odborném periodiku |
Časopis / Zdroj | Bone |
Fakulta / Pracoviště MU | |
Citace | |
Obor | Genetika a molekulární biologie |
Klíčová slova | FGFR3; Oncogene; Skeletal dysplasia; Cartilage; MAP kinase; Senescence |
Popis | FGFR3 signaling is capable of inducing premature senescence in chondrocytes, manifested as reversible, ERK-dependent growth arrest accompanied by alteration of cellular shape, loss of the extracellular matrix, upregulation of senescence markers (alpha-GLUCOSIDASE, FIBRONECTIN, CAVEOLIN 1, LAMIN A, SM22alpha and TIMP 1), and induction of senescence-associated beta-GALACTOSIDASE activity. Our data support a model whereby FGFR3 signaling inhibits cartilage growth via exploiting cellular response originally designed to eliminate cells harboring activated oncogenes. |
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