FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence

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Authors

KREJČÍ Pavel PROCHÁZKOVÁ Jiřina SMUTNÝ Jiří CHLEBOVÁ Katarína LIN Patricia AKLIAN Anie BRYJA Vítězslav KOZUBÍK Alois WILCOX William R.

Year of publication 2010
Type Article in Periodical
Magazine / Source Bone
MU Faculty or unit

Faculty of Science

Citation
Field Genetics and molecular biology
Keywords FGFR3; Oncogene; Skeletal dysplasia; Cartilage; MAP kinase; Senescence
Description 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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