MAP kinases in chondrocyte differentiation.
The majority of the vertebrate skeleton develops through the process of endochondral ossification and involves successive steps of chondrogenesis, chondrocyte proliferation, and hypertrophic chondrocyte differentiation. Interruption of this program through gene mutations and hormonal or environmental factors contributes to numerous diseases, including growth disorders and chondrodysplasias. While a large number of growth factors and hormones have been implicated in the regulation of chondrocyte biology, relatively little is known about the intracellular signaling pathways involved. Recent data provide novel insights into the mechanisms governing acquisition of new phenotypes within the chondrogenic program and suggest multiple pivotal roles for members of the mitogen-activated protein kinase family and their downstream targets in cartilage development. These data are summarized and discussed here.
Stanton
Lee-Anne
LA
CIHR Group in Skeletal Development and Remodeling, Department of Physiology and Pharmacology, University of Western Ontario, London, ON, Canada.
Underhill
T Michael
TM
Beier
Frank
F
D000818:Animals; D002454:Cell Differentiation; D002455:Cell Division; D019902:Chondrocytes / Q000166:cytology* / Q000473:pathology; D006801:Humans; D006984:Hypertrophy; D048031:JNK Mitogen-Activated Protein Kinases; D020935:MAP Kinase Signaling System; D020928:Mitogen-Activated Protein Kinases / Q000502:physiology*; D048051:p38 Mitogen-Activated Protein Kinases
D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases