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Myostatin and Related Factors Are Involved in Skeletal Muscle Protein Breakdown in Growing Broilers Exposed to Constant Heat Stress.

ABSTRACT: Heat stress has an adverse effect on the development of poultry farming, which has always aroused great concern. This study was carried out to investigate the protein breakdown mechanism responsible for the suppressive effect of constant heat stress on muscle growth in growing broilers. A total of 96, 29-day-old, Arbor Acres male broilers were randomly divided into two groups, a thermoneutral control (21 ± 1 °C, TC) and a heat stress (31 ± 1 °C, HS) group, with six replicates in each group and eight birds in each replicate. The trial period lasted for 14 d, and the trial was performed at 60 ± 7% relative humidity, a wind speed of <0.5 m/s and an ammonia level of <5 ppm. The results showed that the average daily feed intake and average daily gain in the HS group were distinctly lower than those in the TC group (p < 0.05), whereas the HS group showed a significantly increased feed conversion ratio, nitrogen excretion per weight gain and nitrogen excretion per feed intake compared to the TC group (p < 0.05). In addition, the HS group showed a significantly reduced breast muscle yield and nitrogen utilization in the broilers (p < 0.05). The HS group showed an increase in the serum corticosterone level (p < 0.05) and a decrease in the thyroxine levels in the broiler chickens (p < 0.05) compared to the TC group, whereas the HS group showed no significant changes in the serum 3,5,3'-triiodothyronine levels compared to the TC group (p > 0.05). Moreover, the HS group showed increased mRNA expression levels of myostatin, Smad3, forkhead box O 4, muscle atrophy F-box and muscle ring-finger 1, but reduced mRNA expression levels of the mammalian target of rapamycin, the protein kinase B and the myogenic determination factor 1 (p < 0.05). In conclusion, the poor growth performance of birds under constant heat stress may be due to an increased protein breakdown via an mRNA expression of myostatin and related factors.

SUBMITTER: Li X

PROVIDER: S-EPMC8160752 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectiveSkeletal muscle dysfunction is an important comorbidity in patients with chronic obstructive pulmonary disease (COPD), and is associated with poor quality of life and reduced survival, but the mechanisms involved remain elusive. Ferroptosis is a newly discovered type of cell death resulting from iron-dependent lipid peroxide accumulation. The purpose of this study was to examine whether ferroptosis is involved in COPD-associated skeletal muscle dysfunction.MethodsA mouse model of COPD was established after 24 weeks of cigarette smoke (CS) exposure, and mRNA sequencing, hematoxylin-eosin (H&E) staining, immunostaining (IF), RT-PCR, and Western blot were utilized to identify the changes in gastrocnemius muscles. In vitro, C2C12 myotubes were treated with CS extract (CSE) and evaluated for ferroptosis-related molecules. The pathways regulating ferroptosis were then explored in CSE-stimulated myotubes.ResultsCompared with controls, COPD mice showed an enriched ferroptosis pathway. Gpx4 was decreased, while hypoxia-inducible factor (Hif) 2α was increased, at gene and protein levels. A reduced level of GSH, but increased cell death, Fe2+, lipid ROS, LPO, and 4-HNE were observed in COPD mice or in CSE-stimulated C2C12 myotubes, which could be ameliorated by ferroptosis inhibitors. The expression of myostatin (MSTN) was enhanced in COPD mice and CSE-stimulated myotubes. MSTN up-regulated HIF2α expression and led to ferroptosis in myotubes, whereas inhibition of MSTN binding to its receptor or inhibition/knockdown of HIF2α resulted in decreased cell death, and partially restored GPX4 and GSH.ConclusionCS exposure induced ferroptosis in vivo and in vitro. Mechanistically, CS-exposure upregulated MSTN which further induced ferroptosis through HIF2α in skeletal muscles, which may contribute to muscle dysfunction through impairing metabolic capacity and decreasing muscle fiber numbers, revealing a potential novel therapeutic target for COPD-related skeletal muscle dysfunction.

Project description:Eccentric contractions produce a significant degree of inflammation and muscle injury that may increase the expression of myostatin. Due to its anti- oxidant and anti-flammatory effects, circulating 17-? estradiol (E2) may attenuate myostatin expression. Eight males and eight females performed 7 sets of 10 reps of eccentric contractions of the knee extensors at 150% 1-RM. Each female performed the eccentric exercise bout on a day that fell within her mid-luteal phase (d 21-23 of her 28-d cycle). Blood and muscle samples were obtained before and 6 and 24 h after exercise, while additional blood samples were obtained at 48 and 72 h after exercise. Serum E2 and myostatin LAP/propeptide (LAP/pro) levels were determined with ELISA, and myostatin mRNA expression determined using RT-PCR. Data were analyzed with two-way ANOVA and bivariate correlations (p < 0.05). Females had greater levels of serum E2 throughout the 72- h sampling period (p < 0.05). While males had greater body mass and fat-free mass, neither was correlated to the pre-exercise levels of myostatin mRNA and LAP/pro for either gender (p > 0.05). Compared to pre-exercise, males had significant increases (p < 0.05) in LAP/propetide and mRNA of 78% and 28%, respectively, at 24 h post-exercise, whereas females underwent respective decreases of 10% and 21%. E2 and LAP/propeptide were correlated at 6 h (r = -0.804, p = 0.016) and 24 h post- exercise (r = -0.841, p = 0.009) in males, whereas in females E2 levels were correlated to myostatin mRNA at 6 h (r =0.739, p = 0.036) and 24 h (r = 0.813, p = 0.014) post-exercise and LAP/propeptide at 6 h (r = 0.713, p = 0.047) and 24 h (r = 0.735, p = 0.038). In females, myostatin mRNA expression and serum LAP/propeptide levels do not appear to be significantly up-regulated following eccentric exercise, and may be due to higher levels of circulating E2. Key PointsThe pre-exercise levels of myostatin mRNA and propeptide were not significantly different between genders, and even though the total body mass and fat-free mass of males were significantly greater than females, neither was correlated to myostatin mRNA or LAP/propeptide.Myostatin mRNA expression in females is less than in males 24 h after a single bout of eccentric exercise.Myostatin LAP/propeptide levels in females are lower in females than in males 24 h after a single bout of eccentric exercise, thereby suggesting a gender-specific mechanism in which females may be less responsive to eccentric exercise than males.Myostatin mRNA expression in females is attenuated, possibly due to inhibition in myostatin signaling, and appears to be more related to the presence of a higher level of circulating E2 rather than body composition.Due to their higher level of E2, females seem to be less susceptible to the mechanism by which eccentric exercise apparently up-regulates myostatin mRNA expression in males.

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Myostatin and Related Factors Are Involved in Skeletal Muscle Protein Breakdown in Growing Broilers Exposed to Constant Heat Stress.

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