High impact information on CHM-I

• Purified ChM-I inhibited DNA synthesis and proliferation of vascular endothelial cells as well as tube morphogenesis in vitro [1].
• Recombinant ChM-I stimulated DNA synthesis and proteoglycan synthesis of cultured growth plate chondrocytes, but inhibited tube morphogenesis of endothelial cells [1].
• These results suggest a regulatory role of ChM-I in vascular invasion during endochondral bone formation [1].
• Expression of ChM-I cDNA in COS7 cells indicated that mature ChM-I molecules were secreted from the cells after post-translational modifications and cleavage from the transmembrane precursor at the predicted processing signal [1].
• The N-terminal amino acid sequence indicated that the inhibitor was identical to chondromodulin I (ChM-I), a cartilage-specific growth-modulating factor [1].

Biological context of CHM-I

• Bovine chondromodulin-I cDNA revealed that the mature protein consists of 121 amino acids with three possible glycosylation sites and is coded as the C-terminal part of a larger precursor [2].
• These results suggest that ChM-I participates in an autocrine signaling mechanism for the anchorage-independent growth of chondrocytes in vitro [3].

Anatomical context of CHM-I

• Molecular cloning of a new class of cartilage-specific matrix, chondromodulin-I, which stimulates growth of cultured chondrocytes [2].
• Chondromodulin-I purified from fetal bovine cartilage markedly stimulated DNA synthesis of cultured growth-plate chondrocytes in the presence of basic fibroblast growth factor (FGF) [2].
• Stimulation of osteoblast proliferation by the cartilage-derived growth promoting factors chondromodulin-I and -II [4].

Associations of CHM-I with chemical compounds

• A glycosylated protein (small, cartilage-derived glycoprotein, SCGP) of approximately 18 kDa with unknown function has been isolated from dissociative extracts of bovine nasal cartilage and its primary structure determined [5].
• Here we purified the inhibitory activity in the 10-50 kDa fraction of guanidine extracts from fetal bovine epiphyseal cartilage, and found that the inhibitor was identical with chondromodulin-I (ChM-I) [6].

Other interactions of CHM-I

• ChM-I alone weakly stimulated the formation of chondrocyte colonies, but it markedly stimulated colony formation synergistically in the presence of an optimal dose of FGF-2 [3].

Analytical, diagnostic and therapeutic context of CHM-I

• On northern blot analysis, expression of chondromodulin-I mRNA was observed only in cartilage [2].
• In situ hybridization and immunohistochemical studies indicated that ChM-I is specifically expressed in the avascular zone of cartilage in developing bone, but not present in calcifying cartilage [1].

References