Enhanced TGF-β signaling and fibrosis in pectoralis major muscle of broiler chicken affected by wooden breast myopathy

ABSTRACT Fibrosis has also been recorded as a prominent pathological feature within wooden breast (WB) myopathy of broiler chicken. This study was conducted to evaluate the accumulation of fibril collagen, deposition of extracellular matrix (ECM) components as well as the underlying mechanism mediating the pathogenic fibrotic process in pectoralis major (PM) muscle of WB affected birds. Broiler chickens were categorized into control and WB groups based on the evaluation of myopathic lesions. Results indicated that total content and area of collagen in cross-sections of PM muscle were greatly increased in WB birds, as well as the augmented expression of collagen-I and fibronectin in the ECM. WB myopathy upregulated expressions of transforming growth factor-beta (TGF-β) and the phosphorylation of Smad2/3 thereby activating TGF-β/Smad signaling pathway, which further enhanced the transcription of pro-fibrotic mediators. Additionally, regulators involved in collagen biosynthesis and crosslinking including prolyl 4-hydroxylase, lysyl oxidase, lysyl hydroxylase and decorin were increased in WB muscle. Finally, the expressions of both matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) were increased in WB muscle, which might be related with reduced ECM remodeling. Overall, WB myopathy induces severe fibrosis by enhancing ECM deposition and collagen crosslinking in PM muscle of broiler chickens, possibly via the activation of TGF-β signaling and the dysregulation of MMP/TIMP system.