Résumé
In fast-growing chicken, the white-striping (WS) myopathy is described macroscopically as white striations parallel to the muscle fiber axis with unknown etiology. These myopathies are described in fast-growing (FG) commercial broilers and affect principally the breast Pectoralis Major (PM) muscle. Muscles are generally categorized in three classes: WS0 corresponding to the absence of macroscopic defect, WS1 for muscles moderately affected by WS, and WS2 for muscle severely affected by the defect. The aim of the present study was to evaluate the role of satellite cells and fibro-adipogenic precursors (FAPs) in the development of the WS physiopathology. This was performed by comparing a slow-growing (SG) chicken line, free of the defect, and a FG chicken line whose muscles are frequently affected by the defect. A histological characterization was performed at 42 days of age on the PM muscle of both lines. As expected, SG muscles appeared histologically normal (absence of any injuries) and served as control. Despite 4 FG chickens were classified as WS0, all muscles of this line (n=8) showed injuries like necrosis-regeneration, extension of perimysial and endomysial connective tissue, and infiltration of adipose tissue at various degrees. To assess the macroscopic phenotypic variability we performed quantitative measurements based on immunohistochemistry and/or western blot expression of different markers (i.e. collagen VI and BODIPY 493 for connective tissue and adipose tissue extension, respectively). We observed in the FG line an increase in muscle fiber size, necrotic and regenerative cell proportion, fibrosis and adiposis compared to SG line. These changes were associated with an increase in Pax7/100 fiber ratio and in nuclei percentage in PDGFRA-positive cells (i.e., FAPs). These preliminary results suggest a role of satellite cells and FAPs in the setting up of the WS myopathy. They will be completed by several in vitro and in vivo measurements to assess the proliferation and differentiation abilities of myogenic precursors and FAPs issued of normal and affected muscles, with the objective to improve our knowledge of the WS physiopathology.