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Effects of corticosterone on the metabolic activity of cultured chicken chondrocytes.

ABSTRACT: Corticosterone is one of the most crucial glucocorticoids (GCs) in poultry. Our previous study shows that corticosterone can retard the longitudinal growth of bones by depressing the proliferation and differentiation of chondrocytes in broilers. The present study was designed to investigate whether corticosterone affect the development of chondrocytes and the synthesis of collagen in vitro. The chondrocytes were isolated from proximal tibial growth plates of 6-week-old broiler chickens and cultured with different doses of corticosterone for 48 h. Then the cell viability, alkaline phosphatase (ALP) activity and the expression of parathyroid hormone-related peptide (PTHrP) and type X collagen (Col X) were detected.At 10(-9)-10(-6) M concentration, corticosterone significantly inhibited the viability and differentiation of chondrocytes, as indicated by decreases in ALP and type X collagen expression. Conversely, there was completely opposite effect at 10(-10) M. In addition, the expression of PTHrP was significantly downregulated at 10(-6) M and 10(-8) M, and was upregulated at 10(-10) M.The results suggested that corticosterone regulated chicken chondrocytes performance depending on its concentration with high concentrations inhibiting the viability and differentiation of chondrocytes and light concentrations promoting them, and these roles of corticosterone may be in part mediated through PTHrP.

SUBMITTER: Zhang H

PROVIDER: S-EPMC4393584 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature

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Effects of corticosterone on the metabolic activity of cultured chicken chondrocytes.

Zhang Hua H Zhou Zhenlei Z Luo Jingwen J Hou Jiafa J

BMC veterinary research 20150408

<h4>Background</h4>Corticosterone is one of the most crucial glucocorticoids (GCs) in poultry. Our previous study shows that corticosterone can retard the longitudinal growth of bones by depressing the proliferation and differentiation of chondrocytes in broilers. The present study was designed to investigate whether corticosterone affect the development of chondrocytes and the synthesis of collagen in vitro. The chondrocytes were isolated from proximal tibial growth plates of 6-week-old broiler ...[more]

PMID: 25880747

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Project description:UnlabelledChondrocytes express RANKL, but their role in osteoclastogenesis is not clear. We report that hypertrophic chondrocytes induce osteoclast formation through RANKL production stimulated by BMP2 and Runx2/Smad1 and thus they may regulate resorption of calcified matrix by osteoclasts at growth plates.IntroductionBone morphogenetic protein (BMP) signaling and Runx2 regulate chondrogenesis during bone development and fracture repair and RANKL expression by osteoblast/stromal cells. Chondrocytes express RANKL, and this expression is stimulated by vitamin D3, but it is not known if chondrocytes directly support osteoclast formation or if BMPs or Runx2 is involved in this potential regulation of osteoclastogenesis.Material and methodsThe chondrocyte cell line, ATDC5, primary mouse sternal chondrocytes, and chick sternal chondrocytes were used. Cells were treated with BMP2, and expression of RANKL and chondrocyte marker genes was determined by real-time RT-PCR and Western blot. Chondrocytes and spleen-derived osteoclast precursors +/- BMP2 were co-cultured to examine the effect of chondrocyte-produced RANKL on osteoclast formation. A reporter assay was used to determine whether BMP2-induced RANKL production is through transcriptional regulation of the RANKL promoter and whether it is mediated by Runx2.ResultsBMP2 significantly increased expression of RANKL mRNA and protein in all three types of chondrocytes, particularly by Col X-expressing and upper sternal chondrocytes. Chondrocytes constitutively induced osteoclast formation. This effect was increased significantly by BMP2 and prevented by RANK:Fc. BMP2 significantly increased luciferase activity of the RANKL-luc reporter, and Smad1 increased this effect. Deletion or mutation of Runx2 binding sites within the RANKL promoter or overexpression of a dominant negative Runx2 abolished BMP2- and Smad1-mediated activation of RANKL promoter activity.ConclusionsHypertrophic chondrocytes may regulate osteoclastogenesis at growth plates to remove calcified matrix through BMP-induced RANKL expression.

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Effects of corticosterone on the metabolic activity of cultured chicken chondrocytes.

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Effects of corticosterone on the metabolic activity of cultured chicken chondrocytes.

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