Transcription profiling of mouse tibia from E15.5 day cultured in minimal media in the presence of vehicle, BSA/HCl (1mM), or C-type natriuretic peptide, CNP (10-6M) reveals C-type natriuretic peptide regulates endochondral ossification through p38 MAP kinase-dependent pathways_2

ABSTRACT: C-type natriuretic peptide (CNP) has been recently identified as an important anabolic regulator of endochondral bone growth, but the molecular mechanism mediating these effects are not completely understood. Here we demonstrate that CNP activates the p38 MAP kinase pathway in chondrocytes and that pharmacological inhibition of p38 blocks the anabolic effects of CNP in a tibia organ culture system. We further show that CNP stimulates endochondral bone growth largely through expansion of the hypertrophic zone of the growth plate, while delaying mineralization. Both effects are reversed by p38 inhibition. We performed Affymetrix microarray analyses to identify CNP target genes in the organ culture system. These studies confirmed that hypertrophic chondrocytes are the main targets of CNP sign

ORGANISM(S): Mus musculus

SUBMITTER: Claudine James 

PROVIDER: E-GEOD-4481 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress