TY - JOUR
T1 - Characterization of wooden breast myopathy
T2 - a focus on syndecans and ECM remodeling
AU - Pejšková, Lucie
AU - Rønning, Sissel Beate
AU - Kent, Matthew Peter
AU - Solberg, Nina Therese
AU - Høst, Vibeke
AU - Thu-Hien, To
AU - Wold, Jens Petter
AU - Lunde, Marianne
AU - Mosleth, Ellen
AU - Pisconti, Addolorata
AU - Kolset, Svein Olav
AU - Carlson, Cathrine Rein
AU - Pedersen, Mona Elisabeth
N1 - Publisher Copyright:
Copyright © 2023 Pejšková, Rønning, Kent, Solberg, Høst, Thu-Hien, Wold, Lunde, Mosleth, Pisconti, Kolset, Carlson and Pedersen.
PY - 2023
Y1 - 2023
N2 - Introduction: The skeletal muscle deformity of commercial chickens (Gallus gallus), known as the wooden breast (WB), is associated with fibrotic myopathy of unknown etiology. For future breeding strategies and genetic improvements, it is essential to identify the molecular mechanisms underlying the phenotype. The pathophysiological hallmarks of WB include severe skeletal muscle fibrosis, inflammation, myofiber necrosis, and multifocal degeneration of muscle tissue. The transmembrane proteoglycans syndecans have a wide spectrum of biological functions and are master regulators of tissue homeostasis. They are upregulated and shed (cleaved) as a regulatory mechanism during tissue repair and regeneration. During the last decades, it has become clear that the syndecan family also has critical functions in skeletal muscle growth, however, their potential involvement in WB pathogenesis is unknown. Methods: In this study, we have categorized four groups of WB myopathy in broiler chickens and performed a comprehensive characterization of the molecular and histological profiles of two of them, with a special focus on the role of the syndecans and remodeling of the extracellular matrix (ECM). Results and discussion: Our findings reveal differential expression and shedding of the four syndecan family members and increased matrix metalloproteinase activity. Additionally, we identified alterations in key signaling pathways such as MAPK, AKT, and Wnt. Our work provides novel insights into a deeper understanding of WB pathogenesis and suggests potential therapeutic targets for this condition.
AB - Introduction: The skeletal muscle deformity of commercial chickens (Gallus gallus), known as the wooden breast (WB), is associated with fibrotic myopathy of unknown etiology. For future breeding strategies and genetic improvements, it is essential to identify the molecular mechanisms underlying the phenotype. The pathophysiological hallmarks of WB include severe skeletal muscle fibrosis, inflammation, myofiber necrosis, and multifocal degeneration of muscle tissue. The transmembrane proteoglycans syndecans have a wide spectrum of biological functions and are master regulators of tissue homeostasis. They are upregulated and shed (cleaved) as a regulatory mechanism during tissue repair and regeneration. During the last decades, it has become clear that the syndecan family also has critical functions in skeletal muscle growth, however, their potential involvement in WB pathogenesis is unknown. Methods: In this study, we have categorized four groups of WB myopathy in broiler chickens and performed a comprehensive characterization of the molecular and histological profiles of two of them, with a special focus on the role of the syndecans and remodeling of the extracellular matrix (ECM). Results and discussion: Our findings reveal differential expression and shedding of the four syndecan family members and increased matrix metalloproteinase activity. Additionally, we identified alterations in key signaling pathways such as MAPK, AKT, and Wnt. Our work provides novel insights into a deeper understanding of WB pathogenesis and suggests potential therapeutic targets for this condition.
KW - broiler chicken
KW - extracellular matrix
KW - myopathy
KW - syndecans
KW - wooden breast
UR - https://www.scopus.com/pages/publications/85180125698
U2 - 10.3389/fphys.2023.1301804
DO - 10.3389/fphys.2023.1301804
M3 - Article
AN - SCOPUS:85180125698
SN - 1664-042X
VL - 14
JO - Frontiers in Physiology
JF - Frontiers in Physiology
M1 - 1301804
ER -