Development of avian tibial dyschondroplasia: gene expression and protein synthesis.

Age-dependent gene expression and protein synthesis associated with chondrocyte differentiation were evaluated in the epiphyseal growth plates of normal and tibial dyschondroplasia (TD)-afflicted chickens. In the normal growth plate, collagen type II gene is expressed mainly by chondrocytes at the upper zone of the growth plate and by the chondrocytes in the articular cartilage. Collagen type X and osteopontin (OPN) genes are expressed in the lower zone of the growth plate and in the zone of cartilage-to-bone transition.

Halofuginone, a specific inhibitor of collagen type I synthesis, prevents dimethylnitrosamine-induced liver cirrhosis.

Background/aims: Hepatic cirrhosis is characterized by excessive deposition of collagen, resulting from an increase in type I collagen gene transcription. We evaluated the effect of halofuginone-a specific inhibitor of collagen type alpha 1(I) gene expression-on dimethylnitrosamine (DMN)-induced liver fibrosis/cirrhosis in rats.

Methods: Fibrosis was induced by intraperitoneal injection of DMN.

Gene expression during cartilage differentiation in turkey tibial dyschondroplasia, evaluated by in situ hybridization.

Gene expression and alkaline phosphatase (AP) activity, associated with chondrocyte differentiation, were evaluated in the epiphyses of normal and tibial dyschondroplasia (TD)-afflicted turkeys. In the normal turkey growth plate (GP), osteopontin (OPN) and type X collagen genes were expressed by the hypertrophic cells in both GP and secondary ossification center, parallel to manifestation of AP activity. Collagen type II gene expression was restricted to the nonhypertrophic chondrocytes at the upper part of the GP.

The expression of estrogen receptor and estrogen effect in MBA-15 marrow stromal osteoblasts.

MBA-15, a marrow stromal-derived cell line, was shown to express an estrogen receptor. This finding was confirmed by in situ hybridization and receptor binding assay. An exposure to estrogen (10(-12)-10(-6) M) in a dose response manner resulted in a decrease of cell proliferation as measured by MTT assay.