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

0345306 - BFÚ 2011 RIV US eng J - Článek v odborném periodiku
Krejčí, Pavel - Procházková, J. - Smutný, J. - Chlebová, K. - Lin, P. - Aklian, A. - Bryja, Vítězslav - Kozubík, Alois - Wilcox, W.R.
FGFR3 signaling induces a reversible senescence phenotype in chondrocytes similar to oncogene-induced premature senescence.
Bone. Roč. 47, č. 1 (2010), s. 102-110. ISSN 8756-3282. E-ISSN 1873-2763
Grant ostatní: GA ČR(CZ) GA301/09/0587
Výzkumný záměr: CEZ:AV0Z50040507; CEZ:AV0Z50040702
Klíčová slova: FGFR3 * oncogene * skeletal dysplasia
Kód oboru RIV: BO - Biofyzika
Impakt faktor: 4.601, rok: 2010

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.
Trvalý link: http://hdl.handle.net/11104/0186614