Myostatin Expression Research Articles

Kidney bean protein hydrolysate as a fish meal replacer: Effects on growth, digestive enzymes, metabolic functions, immune-antioxidant parameters and their related gene expression, intestinal and muscular gene expression

A feeding trial for 70 days was designated on Nile tilapia, Oreochromis niloticus (O. niloticus). A total of 200 fish (34.38 ± 0.05 g) were assigned into five groups, four replicates for each (10 fish/replicate; 40 fish/group) and received five isonitrogenous and isocaloric diets with five replacement levels of fishmeal (FM) with kidney bean (Phaseolus vulgaris L) protein hydrolysate (KBH) (0, 25, 50, 75, 100%). The findings demonstrated a significant increase in the performance metrics (final body weight, total weight gain, average daily weight gain, protein efficiency ratio, and specific growth rate) with a considerable improvement in the feed conversion ratio across all replacement levels, with the greatest value obtained in the KBH75 and KBH100 groups. Regarding the broken line regression analysis, the optimum FM replacement level with KBH was 76%. By replacing FM with KBH, the growth hormone and digestive enzymes (amylase and protease) levels were significantly increased, whilst the glucose and leptin hormone levels significantly declined. The amino acid transporters (solute carrier family 15 member 2 and solute carrier family 26 member 6), insulin growth factor-1, the immune-associated genes (interleukin-8, toll-like receptors-7, and cc-chemokine), and the antioxidant-associated genes (glutathione peroxidase, superoxide dismutase, and Glutathione synthetase) expression was substantially boosted in all replacement levels, where the KBH50 group recorded the highest expression. As well as the mRNA expression of myostatin was down-turned in all replacement levels relative to the KBH0 group. Improving the immune functions (lysozyme, complement 3, nitric oxide, phagocytic %, and phagocytic index) was noticed by FM replacement with KBH. The cumulative mortality as a result of challenging with Aeromonas sobria at the end of the feeding trial was decreased by increasing the replacement level (80, 40, 37, 30, and 25% for KBH0, KBH25, KBH50, KBH75, and KBH100, respectively). From the economic point of view, the feed costs and feed cost/ kg gain declined in the KBH75 and KBH100 diets. From the aforementioned outcomes, KBH could replace the FM up to 100% with improving the growth and their related genes expression, digestive enzymes activity, and immune/antioxidant parameters and their encoding gene expression, and the optimal replacement level was 76%. The replacement of FM with KBH was economically efficient.

Effects of Atmospheric Ammonia on Skeletal Muscle Growth in Broilers

Ammonia, one of the most polluted gases in poultry houses, has always been an urgent problem to solve. Exposure to ammonia can threaten the respiratory tract, induce inflammation, and decrease growth performance. To date, there are few studies investigating the effects of ammonia on skeletal muscle growth. In this experiment, a total of 144 broilers were randomly divided into two groups, and 0 ppm and 35 ppm atmospheric ammonia were administered in the chambers. The trial lasted for 21 days. The breast muscle, thigh muscle, dressed weight, and serum biochemical indexes were measured. The skeletal muscle fibre morphology was observed using light microscopy, and the expressions of genes associated with skeletal muscle development and myosin heavy chain genes were assessed. After 7 days of ammonia exposure, the broilers’ weight in the ammonia group decreased. On the 21st day of the experiment, in the ammonia group, the breast muscle weight, thigh muscle weight, and dressed weight decreased, the blood urea nitrogen content increased, skeletal muscle fibre diameter shortened, the expression of myostatin increased, and the expression of myosin heavy chain-FWM and myosin heavy chain-FRM decreased significantly. This article suggests that 35 ppm atmospheric ammonia seriously affects the skeletal muscle gain rate of broilers, and the myostatin pathway could be a potential regulation of the growth rate of muscle fibre under ammonia exposure.

Effects of Creatine Supplementation on the Myostatin Pathway and Myosin Heavy Chain Isoforms in Different Skeletal Muscles of Resistance-Trained Rats

Creatine has been used to maximize resistance training effects on skeletal muscles, including muscle hypertrophy and fiber type changes. This study aimed to evaluate the impact of creatine supplementation on the myostatin pathway and myosin heavy chain (MyHC) isoforms in the slow- and fast-twitch muscles of resistance-trained rats. Twenty-eight male Wistar rats were divided into four groups: a sedentary control (Cc), sedentary creatine supplementation (Cr), resistance training (Tc), and resistance training combined with creatine supplementation (Tcr). Cc and Tc received standard commercial chow; Cr and Tcr received a 2% creatine-supplemented diet. Tc and Tcr performed a resistance training protocol on a ladder for 12 weeks. Morphology, MyHC isoforms, myostatin, follistatin, and ActRIIB protein expressions were analyzed in soleus and white gastrocnemius portion samples. The results were analyzed using two-way ANOVA and Tukey’s test. Tc and Tcr exhibited higher performance than their control counterparts. Resistance training increased the ratio between muscle and body weight, the cross-sectional area, as well as the interstitial collagen fraction. Resistance training alone increased MyHC IIx and follistatin while reducing myostatin (p < 0.001) and ActRIIB (p = 0.040) expressions in the gastrocnemius. Resistance training induced skeletal muscle hypertrophy and interstitial remodeling, which are more evident in the gastrocnemius muscle. The effects were not impacted by creatine supplementation.

Effects of Enzymatic Hydrolysis and Size Fractionation of Mealworm (Tenebrio molitor larvae) Protein on Antioxidant and Anti-Inflammatory Activities and Inhibition of Muscle Loss

The antioxidant, anti-inflammatory, and muscle loss inhibitory effects of mealworm protein were investigated. Mealworm protein hydrolysate (MPH) was obtained by enzymatic hydrolysis and fractionated based on the molecular size. Although the protein content decreased with hydrolysis, it increased with an increase in size. Upon hydrolysis, essential and branched-chain amino acids decreased while free amino acids increased but decreased with an increase in size. The antioxidant activity increased upon hydrolysis and with an increase in molecular size. The anti-inflammatory effects were highest for MPH > 10 kDa and were similar to whey protein isolate (WPI), for IL-1β, IL-6, and TNF-α. Size fractionation did not significantly affect the anti-inflammatory effects. The MPH > 10 kDa (1.19-fold of control) resulted in the lowest myostatin expression in C2C12 muscle cells with and without LPS, which was similar to WPI (1.23-fold). Consequently, MPH may be a potential alternative to WPI.

Treatment with fibroblast growth factor 19 increases skeletal muscle fiber size, ameliorates metabolic perturbations and hepatic inflammation in 5/6 nephrectomized mice

Chronic kidney disease (CKD) is associated with osteosarcopenia, and because a physical decline in patients correlates with an increased risk of morbidity, an improvement of the musculoskeletal system is expected to improve morbi-mortality. We recently uncovered that the intestinal hormone Fibroblast Growth Factor 19 (FGF19) is able to promote skeletal muscle mass and strength in rodent models, in addition to its capacity to improve glucose homeostasis. Here, we tested the effects of a treatment with recombinant human FGF19 in a CKD mouse model, which associates sarcopenia and metabolic disorders. In 5/6 nephrectomized (5/6Nx) mice, subcutaneous FGF19 injection (0.1 mg/kg) during 18 days increased skeletal muscle fiber size independently of food intake and weight gain, associated with decreased gene expression of myostatin. Furthermore, FGF19 treatment attenuated glucose intolerance and reduced hepatic expression of gluconeogenic genes in uremic mice. Importantly, the treatment also decreased gene expression of liver inflammatory markers in CKD mice. Therefore, our results suggest that FGF19 may represent a novel interesting therapeutic strategy for a global improvement of sarcopenia and metabolic complications in CKD.

Myostatin silencing inhibits podocyte apoptosis in membranous nephropathy through Smad3/PKA/NOX4 signaling pathway.

This article focuses on deciphering the effect of myostatin (MSTN) on podocyte apoptosis in membranous nephropathy (MN) and fathoming out its underlying mechanism. Rats received the intravenous injection of cationized-bovine serum albumin to induce MN in vivo, while angiotensin II (Ang II) was exposed to AB8/13 cells to induce MN model in vitro. The mRNA expression of MSTN was detected by qRT-PCR. The effects of MSTN silencing on MN model rats and cells were assessed by cell counting kit-8 assay, flow cytometry, hematoxylin and eosin staining, and TUNEL assay. The expressions of proteins related to apoptosis and Smad3/protein kinase A (PKA)/NADPH oxidase 4 (NOX4) signaling pathway were examined by western blot. As a result, MSTN was highly expressed in MN cell and rat models. Besides, knockdown of MSTN elevated the MN cell viability and dwindled apoptosis rate, as well as attenuated kidney injury in MN rats. Meanwhile, MSTN silencing lessened the expressions of phosphorylated (p)-Smad3 and Nox4, while boosting the p-PKA expression in MN rats and cells. Additionally, Smad3 overexpression reversed the above effects of MSTN silencing on Ang II-induced podocytes. In conclusion, MSTN knockdown restrains the podocyte apoptosis through regulating Smad3/PKA/NOX4 signaling pathway.

Myostatin Overexpression and Smad Pathway in Detrusor Derived from Pediatric Patients with End-Stage Lower Urinary Tract Dysfunction

Cell therapies and tissue engineering approaches using smooth muscle cells (SMCs) may provide treatment alternatives for end-stage lower urinary tract dysfunction (ESLUTD). Myostatin, a negative regulator of muscle mass, is a promising target to improve muscle function through tissue engineering. The ultimate goal of our project was to investigate the expression of myostatin and its potential impact in SMCs derived from healthy pediatric bladders and pediatric ESLUTD patients. Human bladder tissue samples were evaluated histologically, and SMCs were isolated and characterized. The proliferation of SMCs was assessed by WST-1 assay. The expression pattern of myostatin, its pathway and the contractile phenotype of the cells were investigated at gene and protein levels by real-time PCR, flow cytometry, immunofluorescence, WES and gel contraction assay. Our results show that myostatin is expressed in human bladder smooth muscle tissue and in isolated SMCs at gene and protein levels. A higher expression of myostatin was detected in ESLUTD-derived compared to control SMCs. Histological assessment of bladder tissue confirmed structural changes and decreased muscle-to-collagen ratios in ESLUTD bladders. A decrease in cell proliferation and in the expression of key contractile genes and proteins, α-SMA, calponin, smoothelin and MyH11, as well as a lower degree of in vitro contractility was observed in ESLUTD-derived compared to control SMCs. A reduction in the myostatin-related proteins Smad 2 and follistatin, and an upregulation in the proteins p-Smad 2 and Smad 7 were observed in ESLUTD SMC samples. This is the first demonstration of myostatin expression in bladder tissue and cells. The increased expression of myostatin and the changes in the Smad pathways were observed in ESLUTD patients. Therefore, myostatin inhibitors could be considered for the enhancement of SMCs for tissue engineering applications and as a therapeutic option for patients with ESLUTD and other smooth muscle disorders.

The Preventive Effect of Specific Collagen Peptides against Dexamethasone-Induced Muscle Atrophy in Mice.

Muscle atrophy, also known as muscle wasting, is the thinning of muscle mass due to muscle disuse, aging, or diseases such as cancer or neurological problems. Muscle atrophy is closely related to the quality of life and has high morbidity and mortality. However, therapeutic options for muscle atrophy are limited, so studies to develop therapeutic agents for muscle loss are always required. For this study, we investigated how orally administered specific collagen peptides (CP) affect muscle atrophy and elucidated its molecular mechanism using an in vivo model. We treated mice with dexamethasone (DEX) to induce a muscular atrophy phenotype and then administered CP (0.25 and 0.5 g/kg) for four weeks. In a microcomputed tomography analysis, CP (0.5 g/kg) intake significantly increased the volume of calf muscles in mice with DEX-induced muscle atrophy. In addition, the administration of CP (0.25 and 0.5 g/kg) restored the weight of the gluteus maximus and the fiber cross-sectional area (CSA) of the pectoralis major and calf muscles, which were reduced by DEX. CP significantly inhibited the mRNA expression of myostatin and the phosphorylation of Smad2, but it did not affect TGF-β, BDNF, or FNDC5 gene expression. In addition, AKT/mTOR, a central pathway for muscle protein synthesis and related to myostatin signaling, was enhanced in the groups that were administered CP. Finally, CP decreased serum albumin levels and increased TNF-α gene expression. Collectively, our in vivo results demonstrate that CP can alleviate muscle wasting through a multitude of mechanisms. Therefore, we propose CP as a supplement or treatment to prevent muscle atrophy.

Chronic Stress Induces Type 2b Skeletal Muscle Atrophy via the Inhibition of mTORC1 Signaling in Mice

Chronic stress induces psychological and physiological changes that may have negative sequelae for health and well-being. In this study, the skeletal muscles of male C57BL/6 mice subjected to repetitive water-immersion restraint stress to model chronic stress were examined. In chronically stressed mice, serum corticosterone levels significantly increased, whereas thymus volume and bone mineral density decreased. Further, body weight, skeletal muscle mass, and grip strength were significantly decreased. Histochemical analysis of the soleus muscles revealed a significant decrease in the cross-sectional area of type 2b muscle fibers. Although type 2a fibers also tended to decrease, chronic stress had no impact on type 1 muscle fibers. Chronic stress increased the expression of REDD1, FoxO1, FoxO3, KLF15, Atrogin1, and FKBP5, but did not affect the expression of myostatin or myogenin. In contrast, chronic stress resulted in a decrease in p-S6 and p-4E-BP1 levels in the soleus muscle. Taken together, these results indicate that chronic stress promotes muscle atrophy by inhibiting mammalian targets of rapamycin complex 1 activity due to the upregulation of its inhibitor, REDD1.

Luteolin Protects Against Obese Sarcopenia in Mice with High-Fat Diet-Induced Obesity by Ameliorating Inflammation and Protein Degradation in Muscles.

Although sarcopenia is mainly caused by aging, sarcopenia due to obesity has become an emerging issue given the increase in obesity among people of various ages. There are studies on obesity or sarcopenia, our understanding of obesity-mediated sarcopenia is insufficient. Luteolin (LU) has exhibited antiobesity effects, but no studies have investigated the LU effects on antisarcopenia. This study therefore investigated the effects of LU on obese sarcopenia in mice with high-fat diet (HFD)-induced obesity. To evaluate its inhibitory efficacy against obese sarcopenia, 5-week-old mice are fed an HFD supplemented with LU for 20weeks. LU exerts suppressive effects on obesity, inflammation, and protein degradation in the HFD-fed obese mice. It also inhibits lipid infiltration into the muscle and decreases p38 activity and the mRNA expression of inflammatory factors, including TNF-α, Tlr2, Tlr4, MCP1, and MMP2, in the muscle. The suppression of muscle inflammation by LU leads to the inhibition of myostatin, FoxO, atrogin, and MuRF expression. These effects of LU affect inhibition of protein degradation and improvement of muscle function. Here, it demonstrates that LU's antiobesity and antiinflammatory functionality affect inhibition of muscle protein degradation, and consequently, these interactions by LU exerts a protective effect against obese sarcopenia.

Breast muscle white striping and serum corticosterone reduced in broilers exposed to laser environmental enrichment

Genetic selection for breast yields and fewer days to market has inadvertent effects on broiler meat quality. Woody breast (WB) and white striping (WS) are pectoralis major myopathies prevalent in commercial broilers. Effects of voluntary exercise on these disorders, specifically, are unknown. A second-generation laser enrichment device shown to induce activity in Ross 308 and 708 birds was implemented using 1,360 Ross 708 broilers randomly assigned to laser enrichment or control for 49 d. Laser-enriched birds were exposed to 6-min laser periods 4 times daily. Seventy focal birds were gait and contact dermatitis scored weekly. Blood was collected wk 5 to 7 from 56 broilers for serum corticosterone, myoglobin, and troponin. Seventy broilers were sampled for breast muscle width, fillet dimensions, and WB and WS at wk 6 and 7. One and 2-day postmortem, fillet compression force and water-holding capacity were measured. Serum corticosterone was reduced by up to 21% in laser-enriched birds wk 5 to 7 (P < 0.01). Serum myoglobin was increased in laser-enriched broilers by 5% on wk 5 (P < 0.01) but increased in control birds wk 6 to 7 by up to 13% (P < 0.01). Serum troponin was reduced in laser-enriched broilers by 9% at wk 5 (P < 0.01). Laser exposure increased breast width and fillet weight at d 42 by 1.08 cm (P < 0.05) and 30 g (P < 0.05). At d 49, fillet height was increased 0.42 cm in laser-enriched birds (P < 0.05). Laser enrichment reduced severe WS incidence at d 42 by 24% (P < 0.05) and on d 49 by 15% (P < 0.10). Severe WB score was numerically reduced by 11% in laser enrichment on d 42 and 18% on d 49 (P > 0.05). Water-holding capacity was improved in laser-enriched breasts (P < 0.01) and expression of myostatin and insulin-like growth factor 2 were increased on d 49 (P ≤ 0.01. Laser enrichment reduced markers of stress and muscle damage while improving breast muscle quality and is therefore a potential effective enrichment for commercial broilers.

Impacts of supplemental Ginkgo biloba oil on broilers’ growth, blood indices, intestinal and hepatic morphology and expression of growth-related genes

The current work examined the impact of Ginkgo biloba oil (GBO) on growth performance, some biochemical parameters, intestinal and hepatic morphology, economic efficiency and expression of some growth-related genes in broiler chickens. A total of 135 chicks (Cobb 500) were allotted into three groups with 3 replications (15 birds/replicate). The experimental groups included: G1 (control), G2 and G3 were supplemented with GBO in the drinking water (0.25 and 0.5 cm/L), respectively. The GBO was added to the drinking water only for 3 successive weeks. Compared to the other groups, supplementation with 0.25 cm/L GBO significantly (P ≤ 0.05) increased final body weight, overall weight gain, feed intake and water consumption. When 0.25 cm GBO/L was added, that group significantly differed in intestinal villus length (P ≤ 0.05). Birds received 0.25 cm GBO/L had significantly greater blood total albumin and total protein concentrations (P ≤ 0.05), while birds given 0.5 cm GBO/L had higher serum cholesterol and LDL concentrations (P ≤ 0.05). The cost parameters were significantly higher (P ≤ 0.05) in the 0.25 cm GBO/L supplemented group, which exhibited higher total return and net profit. The addition of 0.25 cm GBO/L resulted in higher expression of antioxidant enzymes and insulin-like growth factor while inhibiting the expression of Myostatin in muscles (P < 0.05) compared to the control and those received 0.5 cm GBO/L. In conclusion, broiler chickens that received 0.25 cm GBO/L for 3 consecutive days per week had better performance, intestinal morphology, profitability, and antioxidant status than the control birds.

A Study of the Ameliorative Effect of Gryllus bimaculatus on Sarcopenia

Purpose: Currently, aging-related sarcopenia is considered a serious problem. However, few studies have addressed the treatment or prevention of sarcopenia using Gryllus bimaculatus . Therefore the present study was carried out to determine whether Gryllus bimaculatus has an ameliorative effect on sarcopenia and to study its applicability as a food for sarcopenia in the elderly or in patients with this condition.Methods: The contents of moisture, crude ash, crude protein, crude fat, carbohydrate and minerals were analyzed. The amino acid and fatty acid compositions were analyzed using an automatic amino acid analyzer and gas chromatography, respectively. Cell viability was measured using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. Myostatin expression was investigated in C2C12 cells using a luciferase reporter assay after treatment with a Gryllus bimaculatus extract.Results: The Gryllus bimaculatus powder (GBP), protein extract of Gryllus bimaculatus (PEGB), Gryllus bimaculatus egg (GBE), and egg protein extract of Gryllus bimaculatus (EPGB) were high in essential amino acids, especially branched chain amino acids, and unsaturated fatty acids, and low in carbohydrates. Moreover, Gryllus bimaculatus appeared to have ameliorative effects on sarcopenia by suppressing the mRNA expression of myostatin in C2C12 cells.Conclusion: It is expected that Gryllus bimaculatus will be positive for the development of food materials or to prevent sarcopenia in the elderly or in patients with this condition.

The G protein-coupled receptor ligand apelin-13 ameliorates skeletal muscle atrophy induced by chronic kidney disease.

Targeting of the apelin-apelin receptor (Apj) system may serve as a useful therapeutic intervention for the management of chronic kidney disease (CKD)-induced skeletal muscle atrophy. We investigated the roles and efficacy of the apelin-Apj system in CKD-induced skeletal muscle atrophy. The 5/6-nephrectomized mice were used as CKD models. AST-120, a charcoal adsorbent of uraemic toxins (8 w/w% in diet), or apelin (1μmol/kg) was administered to CKD mice to investigate the mechanism and therapeutic potential of apelin on CKD-induced skeletal muscle atrophy. The effect of indoxyl sulfate, a uraemic toxin, or apelin on skeletal muscle atrophy was evaluated using mouse myoblast cells (C2C12 cells) in vitro. Skeletal muscle atrophy developed over time following nephrectomy at 12weeks, as confirmed by a significant increase of atrogin-1 and myostatin mRNA expression in the gastrocnemius (GA) muscle and a decrease of lower limb skeletal muscle weight (P<0.05, 0.01 and 0.05, respectively). Apelin expression in GA muscle was significantly decreased (P<0.05) and elabela, another Apj endogenous ligand, tended to show a non-significant decrease at 12weeks after nephrectomy. Administration of AST-120 inhibited the decline of muscle weight and increase of atrogin-1 and myostatin expression. Apelin and elabela expression was slightly improved by AST-120 administration but Apj expression was not, suggesting the involvement of uraemic toxins in endogenous Apj ligand expression. The administration of apelin at 1.0μmol/kg for 4weeks to CKD mice suppressed the increase of atrogin-1 and myostatin, increased apelin and Apj mRNA expression at 30min after apelin administration and significantly ameliorated weight loss and a decrease of the cross-sectional area of hindlimb skeletal muscle. This study demonstrated for the first time the association of the Apj endogenous ligand-uraemic toxin axis with skeletal muscle atrophy in CKD and the utility of therapeutic targeting of the apelin-Apj system.

Effects of soy protein hydrolysates on antioxidant activity and inhibition of muscle loss

Peptides show biological activity, and are more easily digested than complex proteins. In the present work, we evaluated the effects of soy hydrolysate on skeletal muscle. Soy protein isolate (SPI) was hydrolysed using 2% Alcalase (SPHA) and Flavourzyme (SPHF) at pH 8 for 3 h at 60°C, and at pH 7 for 3 h at 55°C, respectively. Antioxidant properties (total phenolic content and DPPH activity) and inhibition of muscle loss (myogenin, myosin heavy chain [MyHC], creatine kinase, and myostatin) by the SPI hydrolysates in C2C12 cells were compared with those of SPI. Alcalase produced more hydrolysed soy oligopeptides than Flavourzyme. Enzymatic hydrolysis increased the levels of essential amino acids, particularly in SPHF (2,466.85 mg/L) as compared to SPI (56.08 mg/L). The total phenolic contents of hydrolysates increased from 12.02 mg GAE/g in SPI to 22.87 and 18.67 mg GAE/g in SPHA and SPHF, respectively. The IC50 value of DPPH activity decreased four times after hydrolysis (SPI: 124.38, SPHA: 32.18, and SPHF: 30.21 mg/mL). SPHA and SPHF treatments increased the expression levels of both MyHC1 and MyHC3, as well as creatine kinase activity. A significant increase in MyHC3 expression was observed in SPHF at 10 µg/mL. Soy hydrolysates (SPHA: 93.5% and SPHF: 61%) induced a greater decrease in the expression of myostatin, a muscle reduction marker, than SPI (30.4%). In conclusion, soy hydrolysates may inhibit muscle loss, showing particularly better effects when Alcalase is used for hydrolysis.

PGC-1β modulates catabolism and fiber atrophy in the fasting-response of specific skeletal muscle beds

ObjectiveSkeletal muscle is a pivotal organ for the coordination of systemic metabolism, constituting one of the largest storage site for glucose, lipids and amino acids. Tight temporal orchestration of protein breakdown in times of fasting has to be balanced with preservation of muscle mass and function. However, the molecular mechanisms that control the fasting response in muscle are poorly understood. MethodsWe now have identified a role for the peroxisome proliferator-activated receptor γ coactivator 1β (PGC-1β) in the regulation of catabolic pathways in this context in muscle-specific loss-of-function mouse models. ResultsMuscle-specific knockouts for PGC-1β experience mitigated muscle atrophy in fasting, linked to reduced expression of myostatin, atrogenes, activation of AMP-dependent protein kinase (AMPK) and other energy deprivation signaling pathways. At least in part, the muscle fasting response is modulated by a negative effect of PGC-1β on the nuclear factor of activated T-cells 1 (NFATC1). ConclusionsCollectively, these data highlight the complex regulation of muscle metabolism and reveal a new role for muscle PGC-1β in the control of proteostasis in fasting.

Myostatin is a negative regulator of adult neurogenesis after spinal cord injury in zebrafish.

Intrinsic and extrinsic inhibition of neuronal regeneration obstruct spinal cord (SC) repair in mammals. In contrast, adult zebrafish achieve functional recovery after complete SC transection. While studies of innate SC regeneration have focused on axon regrowth as a primary repair mechanism, how local adult neurogenesis affects functional recovery is unknown. Here, we uncover dynamic expression of zebrafish myostatin b (mstnb) in a niche of dorsal SC progenitors after injury. mstnb mutants show impaired functional recovery, normal glial and axonal bridging across the lesion, and an increase in the profiles of newborn neurons. Molecularly, neuron differentiation genes are upregulated, while the neural stem cell maintenance gene fgf1b is downregulated in mstnb mutants. Finally, we show that human fibroblast growth factor 1 (FGF1) treatment rescues the molecular and cellular phenotypes of mstnb mutants. These studies uncover unanticipated neurogenic functions for mstnb and establish the importance of local adult neurogenesis for innate SC repair.

Preparation of Bacterial Recombinant Myostatin to Induce the Synthesis of Myostatin-Specific Autoantibodies

The myostatin protein, belonging to the family of growth factors, represents a potential target for therapeutic effects in muscular system pathologies. However, this protein is characterized by other beneficial properties. Polymorphisms of the myostatin gene associated with the restriction of its functional activity are useful as genetic markers of meat productivity in farm animals. Blocking the action of myostatin in productive animals can be achieved by inducing the synthesis of specific autoantibodies using recombinant myostatin, possessing sufficient immunogenicity against myostatin as an antigen. A genetic construct was created and an E. coli producer strain with a high level of expression of recombinant myostatin was obtained.

Nutritional Components, Biochemical Characteristics, Enzyme Activities, and Growth Differences of Five Freshwater Fish Species?

Common carp (Cyprinus carpio) is an economically important fish worldwide, with many of its species bred for consumption. However, there are few reports on the comprehensive comparative analysis of the muscle nutritional quality and stress resistance characteristics of different common carp species. In this study, after 15 months of feeding in the same environment, the nutritional components, serum biochemical indices, liver antioxidant and intestinal digestive enzyme activities, and muscle growth-related gene expression were determined in Songpu mirror carp (SPM; Cyprinus carpio Songpumirror), Heilongjiang wild carp (HLJ; Cyprinus carpio haematopirus), cold-resistant strain of purse red carp (CPR; Cyprinus carpio ‘Red purse cold-resistant’), Songhe carp (SH; Cyprinus carpio ‘Songhe’), and Songpu carp (SP; Cyprinus carpio Songpu). Muscle nutrient composition showed that HLJ had a significantly lower crude fat content and higher docosahexaenoic acid (DHA) + eicosapentaenoic acid (EPA) proportion than the other four common carp species (p &lt; 0.05). The contents of lysine (Lys) and aspargine (Asp) were significantly higher in the CPR than in other species (p &lt; 0.05). Serum biochemical parameters showed that total protein (TP), total cholesterol (T-CHO), triglycerides (TG), and low-density lipoprotein (LDL) were significantly lower in SPM than in the other species (p &lt; 0.05). The results of tissue enzyme activity showed that the activities of superoxide dismutase (SOD) and catalase from Micrococcus lysodeikticus (CAT) in the liver were significantly higher, while the activities of lipase (LPS), trypsin (TRS), and α-amylase (α-AMS) in the intestine were significantly the lower in HLJ than in the other species (p &lt; 0.05). In addition, the relative expression levels of growth hormone (GH), growth hormone receptor (GHR), insulin-like growth factor 1 (IGF1), insulin-like growth factor receptor (IGF1R), and myoblast determination factor (MyoD) in SP and SH were significantly higher than those in the other species, while the relative expression of myostatin (MSTN) in HLJ was significantly higher (p &lt; 0.05). Therefore, there were significant differences in muscle nutritional quality, serum biochemical indices, liver, and intestinal enzyme activities, and muscle growth potential among the five species of common carp. This study could provide a theoretical basis for the germplasm evaluation and variety improvement of common carp.

A Novel Muscle Atrophy Mechanism: Myocyte Degeneration Due to Intracellular Iron Deprivation

Muscle atrophy is defined as the progressive degeneration or shrinkage of myocytes and is triggered by factors such as aging, cancer, injury, inflammation, and immobilization. Considering the total amount of body iron stores and its crucial role in skeletal muscle, myocytes may have their own iron regulation mechanism. Although the detrimental effects of iron overload or iron deficiency on muscle function have been studied, the molecular mechanism of iron-dependent muscle atrophy has not been elucidated. Using human muscle tissues and in the mouse rotator cuff tear model, we confirmed an association between injury-induced iron depletion in myocytes and muscle atrophy. In differentiated C2C12 myotubes, the effects of iron deficiency on myocytes and the molecular mechanism of muscle atrophy by iron deficiency were evaluated. Our study revealed that the lower iron concentration in injured muscle was associated with the upregulation of ferroportin, an iron exporter that transports iron out of cells. Ferroportin expression was increased by hypoxia-inducible factor 1α (HIF1α), which is activated by muscle injury, and its expression is controlled by HIF1 inhibitor treatment. Iron deprivation caused myocyte loss and a marked depletion of mitochondrial membrane potential leading to muscle atrophy, together with increased levels of myostatin, the upstream regulator of atrogin1 and muscle RING-finger protein-1 (MuRF1). Myostatin expression under iron deficiency was mediated by an orphan nuclear receptor, dosage-sensitive sex reversal-adrenal hypoplasia congenita critical region on the X chromosome (DAX1).