BMP8A, TGF-β1 regulates chicken chondrocyte proliferation, differentiation, and apoptosis induced by Thiram
BMP8A, TGF-β1 regulates chicken chondrocyte proliferation, differentiation, and apoptosis induced by Thiram
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Objective: Tibial dyschondroplasia (TD) is a metabolic disorder of cartilage that impairs the development of the tibial growth plate in rapidly growing poultry. This study aimed to identify key genes and clarify the molecular mechanisms involved in TD in broiler chickens. The study evaluated the potential effect of vitamin D3 (VD3) in alleviating TD symptoms, focusing particularly on the role of Bone morphogenetic protein 8A (BMP8A) and its interaction with transforming growth factor-β1 (TGF-β1).Methods: Ninety-four broiler chicks were allocated into three groups: healthy control, thiram-induced TD, and thiram-induced with VD3 supplementation. RNA sequencing was performed to identify differentially expressed genes (DEGs) among the groups. Target genes underwent additional validated using molecular biology techniques, such as gene expression analysis and in vitro functional assays on chondrocytes.Results: VD3 effectively mitigated chondrocyte damage induced by thiram. RNA-seq revealed 625 DEGs enriched in pathways such as the TGF-β signaling pathway. Four co-DEGs (BMP8A, COL10A1, SDC3, and SCIN) were closely associated with collagen metabolism and reorganization. Functional assays, such as CCK8, EdU and IHC showed that BMP8A reduced collagen accumulation induced by elevated TGF-β1 levels, promoted the release of collagen types I, II, and X, and facilitated chondrocyte proliferation and differentiation while reducing apoptosis.Conclusion: BMP8A plays a protective role in TD by the regulation of collagen balance and the maintenance of chondrocyte function, especially in the presence of high TGF-β1 levels. VD3 supplementation effectively reduces TD-related damage. The interaction between BMP8A and TGF-β1 may provide a novel therapeutic target for the prevention and treatment of TD in poultry.
Abstract
Objective: Tibial dyschondroplasia (TD) is a metabolic disorder of cartilage that impairs the development of the tibial growth plate in rapidly growing poultry. This study aimed to identify key genes and clarify the molecular mechanisms involved in TD in broiler chick ens. The study evaluated the potential effect of vitamin D3 (VD3 ) in alleviating TD symp toms, focusing particularly on the role of Bone morphogenetic protein 8A (BMP8A) and its interaction with transforming growth factor-β1 (TGF-β1). Methods: Ninety-four broiler chicks were allocated into three groups: healthy control, thi ram-induced TD, and thiram-induced with VD3 supplementation. RNA sequencing was performed to identify differentially expressed genes (DEGs) among the groups. Target genes underwent additional validated using molecular biology techniques, such as gene expression analysis and in vitro functional assays on chondrocytes. Results: VD3 effectively mitigated chondrocyte damage induced by thiram. RNA-seq re vealed 625 DEGs enriched in pathways such as the TGF-β signaling pathway. Four co DEGs (BMP8A, COL10A1, SDC3, and SCIN) were closely associated with collagen metab olism and reorganization. Functional assays, such as CCK8, EdU and IHC showed that BMP8A reduced collagen accumulation induced by elevated TGF-β1 levels, promoted the release of collagen types I, II, and X, and facilitated chondrocyte proliferation and differen tiation while reducing apoptosis. Conclusion: BMP8A plays a protective role in TD by the regulation of collagen balance and the maintenance of chondrocyte function, especially in the presence of high TGF-β1 levels. VD3 supplementation effectively reduces TD-related damage. The interaction be tween BMP8A and TGF-β1 may provide a novel therapeutic target for the prevention and treatment of TD in poultry.