Disease relevance of Lect1

• CONCLUSION: In experimental uremia, expansion of growth cartilage does not result from increased or persistent expression of ChM-I or from reduced VEGF expression at the cartilage-metaphyseal bone interphase [1].
• Expression of the cartilage derived anti-angiogenic factor chondromodulin-I decreases in the early stage of experimental osteoarthritis [2].

High impact information on Lect1

• Chondromodulin-I expression in the growth plate of young uremic rats [1].
• A similar number of chondrocytes per column was positive for ChM-I in the 4 groups [1].
• In accordance with the elongation of the hypertrophic stratum in uremia, the distance (X+/-SEM, microm) between the extracellular ChM-I signal and the metaphyseal end of growth cartilage was higher (P < 0.003) in UREM (236 +/- 40) and UREM-GH (297 +/- 17) than in SAL (92 +/- 7) and SPF (113 +/- 6) [1].
• The effect of recombinant ChM-I on tube morphogenesis of retinal endothelial cells was examined in culture [3].
• Immunoreactive ChM-I was present in these cells and also in the vitreous body [3].

Biological context of Lect1

• The rat ChM-I gene was determined to encode the open reading frame of 334 amino acid residues, and ChM-I mRNA was exclusively expressed in cartilage, eye, and cerebellum in rats [3].
• OBJECTIVE: Chondromodulin-I (ChM-I), a cartilage derived anti-angiogenic factor, has been shown to regulate the vascular invasion during endochondral bone formation [2].

Anatomical context of Lect1

• Western blot analysis detected an approximately 25-kDa band of ChM-I presumed as a secretory form in the aqueous humor and vitreous body and an approximately 37-kDa band as a precursor form in the retina [3].
• Chondromodulin-I expression in rat articular cartilage [4].
• These findings suggest the loss of ChM-I from articular cartilage might be responsible in part for promoting blood vessel invasion into the cartilage during progression of OA [2].
• The expression of ChM-I mRNA was demonstrated in the cornea at one-third less intensity than that in the sclera with choroids and retinal pigment epithelium by ribonuclease protection assay and real-time PCR [5].
• We found immunoreactivity for ChM-I in the epithelial layer but not the stromal layer or endothelial layer in the cornea, in addition to the positive ChM-I immunoreactivity in other sites in the eye such as the sclera, retina, and ciliary body [5].

Other interactions of Lect1

• Co-immunostaining for ChM-I and CD-31 was performed to localize ChM-I and neovascularization in articular cartilage at advanced stage of OA [2].

Analytical, diagnostic and therapeutic context of Lect1

• METHODS: Growth cartilage ChM-I expression was investigated by immunohistochemistry, in situ hybridization, and reverse transcription-polymerase chain reaction (RT-PCR) in growth-retarded young uremic rats (UREM), control rats, fed ad libitum (SAL) or pair-fed with the UREM group (SPF), and uremic rats treated with growth hormone (UREM-GH) [1].
• No differences in ChM-I expression were appreciated by RT-PCR [1].
• Expression and localization of ChM-I in rat eyes were examined by RNase protection assay and in situ hybridization and by immunostaining, using an antibody against a synthetic peptide [3].

References