Disease relevance of Lect1

• However, a significant increase in bone mineral density with lowered bone resorption with respect to formation was unexpectedly found in adult ChM-I(-/-) mice [1].

High impact information on Lect1

• Tnmd-deficient mice did not have changes in tendon vessel density, and mice lacking both Tnmd and ChM-I had normal retinal vascularization and neovascularization after oxygen-induced retinopathy [2].
• It is predominantly expressed in tendons, ligaments, and eyes, whereas the only other family member, chondromodulin I (ChM-I), is highly expressed in cartilage and at lower levels in the eye and thymus [2].
• Chondromodulin I (ChM-I) was supposed from its limited expression in cartilage and its functions in cultured chondrocytes as a major regulator in cartilage development [1].
• No overt abnormality was detected in endochondral bone formation during embryogenesis and cartilage development during growth stages of ChM-I(-/-) mice [1].
• Thus, the present study established that ChM-I is a bone remodeling factor [1].

Biological context of Lect1

• The encoded protein was named myodulin because of sequence homologies with the cartilage-specific chondromodulin-I (ChM-I) protein, its restricted expression in skeletal muscle tissue, and its modulating properties on vascular endothelial cells described here [3].
• Production of a secreted form of TeM and ChM-I through adenoviral gene transfer caused effective autocrine suppression of cell proliferation and capillary-like morphogenesis of retina vascular endothelial cells [4].
• The predicted amino acid sequence revealed 33% overall identity with mouse ChM-I precursor [5].
• Here we cloned the mouse chondromodulin-I cDNA from a mouse whole embryo cDNA library [6].
• These results suggest that chondromodulin-I is involved in the anti-angiogenic property of cartilage, and that the withdrawal of its expression allows the vascular invasion which triggers the replacement of cartilage by bone during endochondral bone development [6].

Anatomical context of Lect1

• Antiangiogenic function included in the C terminus of TeM and ChM-I was examined in vascular endothelial cells through adenoviral gene transduction [4].
• Chondromodulin I (chm-I), a type II transmembrane protein, is highly expressed in the avascular zones of cartilage but is downregulated in the hypertrophic region, which is invaded by blood vessels during enchondral ossification [7].
• Suppression of T cell responses by chondromodulin I, a cartilage-derived angiogenesis inhibitory factor: therapeutic potential in rheumatoid arthritis [8].
• ChM-I is specifically expressed in the avascular regions of the growth-plate and cartilaginous bone rudiments in embryos [9].
• Chondromodulin-I and tenomodulin: a new class of tissue-specific angiogenesis inhibitors found in hypovascular connective tissues [9].

Associations of Lect1 with chemical compounds

• Chondromodulin-I (ChM-I) is a cartilage-specific glycoprotein that stimulates the growth of chondrocytes and inhibits the tube formation of endothelial cells [10].

Analytical, diagnostic and therapeutic context of Lect1

• CONCLUSIONS: These results indicate a potential role for TeM in prevention of vascular invasion in the mouse eye and the possibility of both TeM and ChM-I as candidates for use in gene therapy approaches to treatment of ocular angiogenesis [4].
• METHODS: The localization of ChM-I expression in mouse thymus tissue was examined by in situ hybridization [8].
• Northern blot analysis revealed that the chondromodulin-I transcripts were expressed in association with the formation of cartilage expressing type II collagen from days 11 to 17 of gestation in mouse embryos, at which time cartilaginous bone rudiments were gradually replaced by bone [6].

References