Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.27.1 (RNase)
 16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To define genes specifically expressed in cartilage and during chondrogenesis, we compared by differential display-polymerase chain reaction (DD-PCR) the mRNA populations of differentiated sternal chondrocytes from chicken embryos with mRNA species modulated in vitro by retinoic acid (RA). Chondrocyte-specific gene expression is downregulated by RA, and PCR-amplified cDNAs from both untreated and RA-modulated cells were differentially displayed. Amplification products only from RNA of untreated chondrocytes were further analyzed, and a cDNA-fragment of the chondromodulin-I (ChM-I) mRNA was isolated. After obtaining full length cDNA clones, we have analyzed the mRNA expression patterns at different developmental stages by RNase protection assay and in situ hybridization. Analysis of different tissues and cartilage from 17-day-old chicken embryos showed ChM-I mRNA only in chondrocytes. During somitogenesis of the chicken embryo, ChM-I transcripts were detected in the notochord, the floor and the roof plate of the neural tube, and in cartilage precursor tissues such as the sclerotomes of the somites, the developing limbs, the pharyngeal arches, the otic vesicle, and the sclera. ChM-I continued to be expressed in differentiated cartilages derived from these tissues and also in noncartilaginous domains of the developing heart and retina. Thus, in the chicken, the expression of ChM-I is not restricted to mature cartilage but is already present during early development in precartilaginous tissues as well as in heart and eye.
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PMID:Spatio-temporal distribution of chondromodulin-I mRNA in the chicken embryo: expression during cartilage development and formation of the heart and eye. 1059 Apr 75

The localization and expression of chondromodulin-I (ChM-I), an angiogenesis inhibitor, in the rat articular cartilage during maturation from 2 to 10 weeks of age were examined by immunohistochemistry, Western blot analysis and ribonuclease protection assay, and the results were compared with those in the epiphyseal cartilage. ChM-I was found to be diffusely immunostained in the inter-territorial space of the cartilage matrix from the intermediate to the deep layers at the immature stage. As the articular cartilage matured, the immunoreactivity was localized around the hypertrophic chondrocytes in the deep layer and the immunoreactivity became weak after maturation. In contrast, the ChM-I immunoreactivity was intense in the epiphyseal cartilage at all ages examined. ChM-I was detected by Western blotting as a broad band or occasionally as a cluster of multiple bands (approximately 25 kDa) in both the articular and the epiphyseal cartilage. The intensity of the bands decreased gradually with age in the articular cartilage, but was unchanged in the epiphyseal cartilage at all ages. Ribonuclease protection assay revealed that ChM-I mRNA also decreased gradually with age in the articular cartilage in parallel with the maturation of the articular cartilage, while no decrease in ChM-I mRNA was found in the epiphyseal cartilage. The expression of ChM-I mRNA in the articular cartilage was less than that in the epiphyseal cartilage at all ages. The decrease in amount of ChM-I in the mature articular cartilage suggests that ChM-I plays a more important role in the maintenance of avascularity in the immature articular cartilage than in the mature one. The avascular condition may be preserved by angiogenic inhibitors or mechanisms other than ChM-I in the mature articular cartilage.
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PMID:Chondromodulin-I expression in rat articular cartilage. 1452 63

The localization and expression in the rat cornea of chondromodulin-I (ChM-I), an inhibitory angiogenesis factor, were examined by immunohistochemistry, Western blot analysis, ribonuclease protection assay, and real-time PCR assay. 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. The ChM-I immunoreactivity was most intense at the outside of the basal cells and in their cytoplasm while the intensity of the immunoreactivity decreased gradually from the wing cells to the superficial cells in the corneal epithelial layer. No reactivity however, was detected in the Bowman's membrane or conjunctival epithelial cells which had continuity with the corneal epithelial cells. 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. ChM-I in the corneal epithelial layer may prevent neovascularization and maintain avascularity in the cornea.
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PMID:Localization and expression of chondromodulin-I in the rat cornea. 1501 47