DEVELOPMENT OF AVIAN TIBIAL DYSCHONDROPLASIA - GENE-EXPRESSION AND PROTEIN-SYNTHESIS

Citation
M. Pines et al., DEVELOPMENT OF AVIAN TIBIAL DYSCHONDROPLASIA - GENE-EXPRESSION AND PROTEIN-SYNTHESIS, Calcified tissue international, 63(6), 1998, pp. 521-527
Citations number
39
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0171967X
Volume
63
Issue
6
Year of publication
1998
Pages
521 - 527
Database
ISI
SICI code
0171-967X(1998)63:6<521:DOATD->2.0.ZU;2-6
Abstract
Age-dependent gene expression and protein synthesis associated with ch ondrocyte differentiation were evaluated in the epiphyseal growth plat es of normal and tibial dyschondroplasia (TD)-afflicted chickens. In t he normal growth plate, collagen type II gene is expressed mainly by c hondrocytes at the upper zone of the growth plate and by the chondrocy tes in the articular cartilage. Collagen type X and osteopontin (OPN) genes are expressed in the lower zone of the growth plate and in the z one of cartilage-to-bone transition. No age-dependent changes in the p attern of OPN and collagen type II or X gene expression were observed up to 20 days of age. In the TD-afflicted growth plates, the lesion is enlarged with age, and chondrocytes expressing the collagen type II g ene were observed in the hypertrophic zone as early as 8 days posthatc hing. Abnormal expression of OPN and collagen type X genes was also ob served starting at 13 days of age. At day 20, the entire TD lesion-whi ch was significantly enlarged-was surrounded by collagen type II, coll agen type X, and OPN expressing cells. The level of OPN in TD was redu ced with increasing age, and at 20 days almost no OPN could be detecte d in either the upper or the lower hypertrophic zones. The level of bo ne sialoprotein (BSP) also diminished with increasing age in the TD gr owth plates. In contrast to OPN, the age-dependent reduction in BSP le vels was mainly in the lower hypertrophic zone (LHZ), and at 20 days o f age, BSP was barely detected in the LHZ, whereas in the upper hypert rophic zone, the levels of BSP were similar to those in normal growth plate. In summary, our results suggest that the primary event of the T D lesion occurs in cells of proliferative phenotype within the hypertr ophic zone. These cells divide and form the TD lesion, which consists of cells that do not express the genes associated with hypertrophy.