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The unique physiological features of the broiler pectoralis major muscle as suggested by the three-dimensional ultrastructural study of mitochondria in type IIb muscle fibers.

ABSTRACT: Typical skeletal muscles are composed of mixed muscle fiber types, which are classified as slow-twitch (type I) and fast-twitch (type II) fibers, whereas pectoralis major muscles (PMs) in broiler chickens are 100% composed of type IIb fast-twitch fibers. Since metabolic properties differ among muscle fiber types, the combination of muscle fiber types is involved in physiological functions and pathological conditions in skeletal muscles. In this study, using serial block-face scanning electron microscopy, we compared three-dimensional (3D) mitochondrial properties in type IIb fibers in broiler PMs and those in type I fibers of broiler gastrocnemius muscles (GMs) heterogeneously composed of slow- and fast-twitch muscle fibers. In type I fibers in the GMs, elongated mitochondria with numerous interconnections to form a substantial network among myofibrils were observed. Along with lipid droplets sandwiched by mitochondria, these features are an adaptation to effective oxidative respiration and constant oxidative damage in slow-twitch muscle fibers. In contrast, type IIb fibers in the PMs showed small and ellipsoid-shaped mitochondria with few interconnections and no lipid droplets, forming a sparse network. The mitochondrial spatial network comprises of active mitochondrial dynamics to reduce mitochondrial damage; therefore, type IIb fibers possess physiologically low capacity to maintain mitochondrial wellness due to static mitochondrial dynamics. Based on 3D mitochondrial properties, we discussed the contrasting physiological functions between type I and IIb fibers and proposed a high contractile power and low stress resistance as unique physiological properties of broiler PMs.

SUBMITTER: Hosotani M

PROVIDER: S-EPMC8636870 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Wooden breast syndrome (WB) constitutes an emerging myopathy in the pectoralis major muscle (PM) of broiler chickens, characterized by myofiber hypertrophy and degeneration along with severe fibrosis. WB pathogenesis has been considered to involve hypoxia induced by rapid growth of the PM. In this study, we focused on mitochondrial morphology and dynamics in the myofibers, as these organelles are sensitive to damage by hypoxia, and examined the effects on WB pathogenesis. Specifically, the PMs of a flock of 35 broilers at 50 days of age were evaluated. First, the severity of disease in each bird was determined by measuring histopathological indices including the fibrotic area (FA) in the muscle and circularity of myofibers (CM). These values were 29.4 ± 9.6% and 0.70 ± 0.042, respectively, showing variety among the flock. Myofiber vacuolization was observed in all birds including numerous small- or large-rimmed vacuoles, with the former consisting of ultrastructurally autophagosome-like vacuoles engulfing degenerated mitochondria. The large-rimmed vacuoles frequently occurred in the PMs with more severe FA and CM, indicating a relationship between altered autophagy/mitophagy and WB severity. Next, the expression levels of hypoxia-adaptive and mitochondrial dynamics-related genes were analyzed, and their correlations with the histopathological indices were examined. The histopathological indices were negatively correlated with the expression of vascular endothelial growth factor A (VEGFA), indicating that less angiogenesis owing to weakened hypoxia-inducible factor signaling induces more severe WB pathology. In addition, the observed negative correlation with mitochondrial dynamics-related genes implied that WB pathology deteriorates concomitant with reduced mitochondrial dynamics. Furthermore, the expression of mitochondrial dynamics-related genes showed strong positive correlation with that of VEGFA and autophagy-/mitophagy-related genes. These results revealed that the PMs of broilers possess the mechanism of physiological clearance of mitochondria damaged by the hypoxia resulting from the continuous mitochondrial dynamics and autophagy/mitophagy accompanying rapid PM growth. In turn, the altered mitochondrial clearance induced by chronic hypoxia and the accumulation of damaged mitochondria likely underly the severe pathological features of WB.

Project description:Angiotensin II (ANG II)-induced skeletal muscle wasting is characterized by activation of the ubiquitin-proteasome system. However, the potential involvement of proteolytic system macroautophagy/autophagy in this wasting process remains elusive. Autophagy is precisely regulated to maintain cell survival and homeostasis; thus its dysregulation (i.e., overactivation or persistent suppression) could lead to detrimental outcomes in skeletal muscle. Here we show that infusion of ANG II for 7 days in male FVB mice suppressed autophagy in skeletal muscle. ANG II blunted microtubule-associated protein 1 light chain 3B (LC3B)-I-to-LC3B-II conversion (an autophagosome marker), increased p62/SQSTM1 (an autophagy cargo receptor) protein expression, and decreased the number of autophagic vacuoles. ANG II inhibited UNC-51-like kinase 1 via inhibition of 5'-AMP-activated kinase and activation of mechanistic target of rapamycin complex 1, leading to reduced phosphorylation of beclin-1Ser14 and Autophagy-related protein 14Ser29, suggesting that ANG II impairs autophagosome formation in skeletal muscle. In line with ANG II-mediated suppression of autophagy, ANG II promoted accumulation of abnormal/damaged mitochondria, characterized by swelling and disorganized cristae and matrix dissolution, with associated increase in PTEN-induced kinase 1 protein expression. ANG II also reduced mitochondrial respiration, indicative of mitochondrial dysfunction. Together, these results demonstrate that ANG II reduces autophagic activity and disrupts mitochondrial ultrastructure and function, likely contributing to skeletal muscle wasting. Therefore, strategies that activate autophagy in skeletal muscle have the potential to prevent or blunt ANG II-induced skeletal muscle wasting in chronic diseases. NEW & NOTEWORTHY Our study identified a novel mechanism whereby angiotensin II (ANG II) impairs mitochondrial energy metabolism in skeletal muscle. ANG II suppressed autophagosome formation by inhibiting the UNC-51-like kinase 1(ULK1)-beclin-1 axis, resulting in accumulation of abnormal/damaged and dysfunctional mitochondria and reduced mitochondrial respiratory capacity. Therapeutic strategies that activate the ULK1-beclin-1 axis have the potential to delay or reverse skeletal muscle wasting in chronic diseases characterized by increased systemic ANG II levels.

Project description:The muscle myopathy wooden breast (WB) has recently appeared in broiler production and has a negative impact on meat quality. WB is described as hard/firm consistency found within the pectoralis major (PM). In the present study, we use machine learning from our PM and liver transcriptome dataset to capture the complex relationships that are not typically revealed by traditional statistical methods. Gene expression data was evaluated between the PM and liver of birds with WB and those that were normal. Two separate machine learning algorithms were performed to analyze the data set including the sequential minimal optimization (SMO) of support vector machines (SVMs) and Multilayer Perceptron (MLP) Artificial Neural Network (ANN). Machine learning algorithms were compared to identify genes within a gene expression data set of approximately 16,000 genes for both liver and PM, which can be correctly classified from birds with or without WB. The performance of both machine learning algorithms SMO and MLP was determined using percent correct classification during the cross-validations. By evaluating the WB transcriptome datasets by 5× cross-validation using ANNs, the expression of nine genes ranked based on Shannon Entropy (Information Gain) from PM were able to correctly classify if the individual bird was normal or exhibited WB 100% of the time. These top nine genes were all protein coding and potential biomarkers. When PM gene expression data were evaluated between normal birds and those with WB using SVMs they were correctly classified 95% of the time using 450 of the top genes sorted ranked based on Shannon Entropy (Information Gain) as a preprocessing step. When evaluating the 450 attributes that were 95% correctly classified using SVMs through Ingenuity Pathway Analysis (IPA) there was an overlap in top genes identified through MLP. This analysis allowed the identification of critical transcriptional responses for the first time in both liver and muscle during the onset of WB. The information provided has revealed many molecules and pathways making up a complex molecular mechanism involved with the progression of wooden breast and suggests that the etiology of the myopathy is not limited to activity in the muscle alone, but is an altered systemic pathology.

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The unique physiological features of the broiler pectoralis major muscle as suggested by the three-dimensional ultrastructural study of mitochondria in type IIb muscle fibers.

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