Search Results (8)

To clarify the relationship between muscle development and meat quality in Ziwuling black goats, this study used the longissimus dorsi muscle of 6-month-old and 12-month-old goats as samples. With HE staining, fast–slow myofiber immunofluorescence double staining, and transcriptome sequencing, this study analyzed muscle structure, myofiber type transformation, and molecular regulation. Results showed that 6-month-olds had higher myofiber density and smaller diameter; 12-month-olds showed myofiber hypertrophy (larger diameter); immunofluorescence revealed more fast-twitch myofibers (Type II) at 6 months and increased slow-twitch ones (Type I) at 12 months. Transcriptome sequencing identified 387 differentially expressed genes (DEGs: 156 upregulated, 231 downregulated). GO analysis indicated that DEGs are involved in skeletal muscle growth, cAMP biosynthesis, etc.; KEGG analysis showed enrichment in arginine–proline metabolism and AMPK/MAPK signaling pathways (AMPK regulates fatty acid metabolism genes like ACACB/CPT1A; arginine–proline metabolism relates to muscle maturation). WGCNA clustered genes into nine modules (MEblue correlated with myofiber density/MAPK; MEgreen correlated negatively with diameter but positively with density, involving PPARGC1A/AMPK). In conclusion, protein nutrition at 6 months (promote myofiber proliferation) and regulating energy intake at 12 months (improve meat quality) are recommended, and 12 months is the optimal slaughter age. Full article

Skeletal muscles are essential for movement and support but are vulnerable to injury. Muscle regeneration relies on the extracellular matrix (ECM), which regulates key cellular processes. Transforming growth factor β-induced (TGFBI), an ECM component involved in cell adhesion, migration, and tissue development, has not been investigated in skeletal muscle regeneration. Here, we examined the role of TGFBI using Tgfbi knockout (KO) mice and C2C12 myoblasts. In vitro, C2C12 cells were treated with recombinant TGFBI following snake venom (SV)-induced injury, and myogenic differentiation and fusion were evaluated by quantitative real-time PCR (qRT-PCR) and Western blotting. In vivo, acute muscle injury was induced by SV injection into the tibialis anterior muscles of 12-week-old wild-type and Tgfbi KO mice, with regeneration assessed by histology and qRT-PCR. TGFBI was absent in uninjured muscle and C2C12 cells but was upregulated after injury. Recombinant TGFBI enhanced myogenic differentiation and restored SV-induced downregulation of myogenic and fusion markers. Although phenotypically normal under physiological conditions, Tgfbi KO mice exhibited impaired regeneration, characterized by persistent immature myofibers, elevated inflammatory cytokines, reduced myogenic marker expression, and increased fibrosis. These findings reveal TGFBI as a key regulator of skeletal muscle repair and a potential therapeutic target for muscle-related disorders. Full article

Hemojuvelin (HJV) is a membrane-bound protein prominently expressed in the skeletal muscle, heart, and liver. Despite its established function in iron regulation, the specific role of HJV in muscle physiology and pathophysiology is not well understood. In this study, we explored the involvement of HJV in disuse-induced muscle atrophy and uncovered the potential mechanisms. Hindlimb unloading (HU) resulted in soleus muscle atrophy in wild type (WT) mice, accompanied by a significant decrease in HJV protein expression. The muscle-specific deletion of Hjv (MKO) exacerbated myofiber atrophy, which was associated with an increase in the expression of muscle ubiquitin ligases following HU. Furthermore, the expression of transforming growth factor-β type II receptor (TβRII) and the level of phosphorylated Smad3 (p-Smad3) were elevated after HU, and these effects were exacerbated in MKO mice. The knockdown of TβRII in the skeletal muscle of MKO mice mitigated myofiber atrophy and reversed the hyperactivation of the TβRII/Smad3 pathway induced by HU. Our findings demonstrate that the absence of HJV contributes to the activation of the TβRII/Smad3 signaling pathway and, consequently, the onset of myofiber atrophy in response to HU. Given its abundant expression in skeletal muscle, HJV emerges as a potential therapeutic target for muscle atrophy. Full article

Mechanical ventilation (MV), used in patients with acute lung injury (ALI), induces diaphragmatic myofiber atrophy and contractile inactivity, termed ventilator-induced diaphragm dysfunction. Phosphoinositide 3-kinase-γ (PI3K-γ) is crucial in modulating fibrogenesis during the reparative phase of ALI; however, the mechanisms regulating the interactions among MV, myofiber fibrosis, and PI3K-γ remain unclear. We hypothesized that MV with or without bleomycin treatment would increase diaphragm muscle fibrosis through the PI3K-γ pathway. Five days after receiving a single bolus of 0.075 units of bleomycin intratracheally, C57BL/6 mice were exposed to 6 or 10 mL/kg of MV for 8 h after receiving 5 mg/kg of AS605240 intraperitoneally. In wild-type mice, bleomycin exposure followed by MV 10 mL/kg prompted significant increases in disruptions of diaphragmatic myofibrillar organization, transforming growth factor-β1, oxidative loads, Masson’s trichrome staining, extracellular collagen levels, positive staining of α-smooth muscle actin, PI3K-γ expression, and myonuclear apoptosis (p < 0.05). Decreased diaphragm contractility and peroxisome proliferator-activated receptor-γ coactivator-1α levels were also observed (p < 0.05). MV-augmented bleomycin-induced diaphragm fibrosis and myonuclear apoptosis were attenuated in PI3K-γ-deficient mice and through AS605240-induced inhibition of PI3K-γ activity (p < 0.05). MV-augmented diaphragm fibrosis after bleomycin-induced ALI is partially mediated by PI3K-γ. Therapy targeting PI3K-γ may ameliorate MV-associated diaphragm fibrosis. Full article

The Chuanzang black (CB) pig is a new crossbred between Chinese local breeds and modern breeds. Here, we investigated the growth performance, plasma indexes, carcass traits, and meat quality characteristics of conventional DLY (Duroc × Landrace × Yorkshire) crossbreed and CB pigs. The LC-MS/MS-based metabolomics of pork from DLY and CB pigs, as well as the relationship between the changes in the metabolic spectrum and meat quality, were analyzed. In this study, CB pigs presented lower final body weight, average daily gain, carcass weight, and eye muscle area than DLY pigs (p ˂ 0.05). Conversely, the ratio of feed to gain, marbling score, and meat color score of longissimus dorsi (LD) were higher in CB than DLY pigs (p ˂ 0.05). Moreover, psoas major (PM) showed a higher meat color score and a lower cooking loss in CB than DLY pigs (p ˂ 0.05). Interestingly, CB pigs showed lower myofiber diameter and area but higher myofiber density than DLY pigs (p ˂ 0.05). Furthermore, the mRNA expression levels of MyHC I, PPARδ, MEF2C, NFATC1, and AMPKα1 were higher in CB than DLY pigs (p ˂ 0.05). Importantly, a total of 753 metabolites were detected in the two tissues (e.g., psoas major and longissimus dorsi) of CB and DLY pigs, of which the difference in metabolite profiles in psoas major between crossbreeds was greater than that in longissimus dorsi. Specifically, palmitic acid, stearic acid, L-aspartic acid, corticosterone, and tetrahydrocorticosterone were the most relevant metabolites of psoas major meat quality, and tetrahydrocorticosterone, L-Palmitoylcarnitine, arachidic acid, erucic acid, and 13Z,16Z-docosadienoic acid in longissimus dorsi meat were positively correlated with meat quality. The most significantly enriched KEGG pathways in psoas major and longissimus dorsi pork were galactose metabolism and purine metabolism, respectively. These results not only indicated improved meat quality in CB pigs as compared to DLY pigs but may also assist in rational target selection for nutritional intervention or genetic breeding in the swine industry. Full article

The differences of pork quality characteristics among different pig breeds mainly came from the differences in myofiber type compositions. Growing evidence indicated the key role of miRNAs in myofiber specification. In the present study, we found that miR-152 is more abundant in the slow-twitch myofiber-enriched muscles. However, its role in myofiber type transformation and myogenesis is largely unknown. Overexpression of miR-152 in porcine myotubes promoted the formation of slow-twitch myofibers and myogenesis. While, inhibition of miR-152 expression showed the opposite effect to miR-152 mimics transfection. The luciferase reporter analysis confirmed that miR-152 straightly targets the 3′-untranslated region (3’-UTR) of uncoupling protein 3 (UCP3) to cause its post-transcriptional inhibition in the protein level. The knockdown of UCP3 by siRNA showed the similar effect of miR-152 on myofiber type transition. Furthermore, the rescue experiment in the porcine myotube transfected with miR-152 mimics or/and UCP3 overexpression plasmid with or without the 3’UTR revealed that UCP3 mediates the action of miR-152 in slow-twitch myofiber formation. Taken together, our findings proposed a novel molecular mechanism through which miR-152 epigenetically regulates meat quality via promoting slow-twitch myofiber formation and skeletal myogenesis. Full article

This study investigated the effect of leucine supplementation on the skeletal muscle regenerative process, focusing on the remodeling of connective tissue of the fast twitch muscle tibialis anterior (TA). Young male Wistar rats were supplemented with leucine (1.35 g/kg per day); then, TA muscles from the left hind limb were cryolesioned and examined after 10 days. Although leucine supplementation induced increased protein synthesis, it was not sufficient to promote an increase in the cross-sectional area (CSA) of regenerating myofibers (p > 0.05) from TA muscles. However, leucine supplementation reduced the amount of collagen and the activation of phosphorylated transforming growth factor-β receptor type I (TβR-I) and Smad2/3 in regenerating muscles (p < 0.05). Leucine also reduced neonatal myosin heavy chain (MyHC-n) (p < 0.05), increased adult MyHC-II expression (p < 0.05) and prevented the decrease in maximum tetanic strength in regenerating TA muscles (p < 0.05). Our results suggest that leucine supplementation accelerates connective tissue repair and consequent function of regenerating TA through the attenuation of TβR-I and Smad2/3 activation. Therefore, future studies are warranted to investigate leucine supplementation as a nutritional strategy to prevent or attenuate muscle fibrosis in patients with several muscle diseases. Full article

Molecular biology has enabled the identification of the mechanisms whereby inactive myostatin increases skeletal muscle growth in double-muscled (DM) animals. Myostatin is a secreted growth differentiation factor belonging to the transforming growth factor-β superfamily. Mutations make the myostatin gene inactive, resulting in muscle hypertrophy. The relationship between the different characteristics of DM cattle are defined with possible consequences for livestock husbandry. The extremely high carcass yield of DM animals coincides with a reduction in the size of most vital organs. As a consequence, DM animals may be more susceptible to respiratory disease, urolithiasis, lameness, nutritional stress, heat stress and dystocia, resulting in a lower robustness. Their feed intake capacity is reduced, necessitating a diet with a greater nutrient density. The modified myofiber type is responsible for a lower capillary density, and it induces a more glycolytic metabolism. There are associated changes for the living animal and post-mortem metabolism alterations, requiring appropriate slaughter conditions to maintain a high meat quality. Intramuscular fat content is low, and it is characterized by more unsaturated fatty acids, providing healthier meat for the consumer. It may not always be easy to find a balance between the different disciplines underlying the livestock husbandry of DM animals to realize a good performance and health and meat quality. Full article