scholarly journals Characterization of two myostatin genes in pufferfish Takifugu bimaculatus: sequence, genomic structure, and expression

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9655
Author(s):  
Yinzhen Sheng ◽  
Yulong Sun ◽  
Xin Zhang ◽  
Haifu Wan ◽  
Chengjie Yao ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Genomic Structure ◽  
Muscle Growth ◽  
Negative Regulator ◽  
Pigment Formation ◽  
Formation Stage ◽  
Proliferation And Differentiation ◽  
The Brain

Myostatin (MSTN) is a negative regulator of muscle growth, which restrains the proliferation and differentiation of myoblasts. To understand the role of two mstn genes of Takifugu bimaculatus, the full-length cDNAs of 1131 bp Tbmstn1 and 1,080 bp Tbmstn2 were obtained from the T. bimaculatus’ genomic database, which encodes 376 and 359 amino acids, respectively. The results of qRT-PCR showed that Tbmstn1 was expressed in the eye, kidney, spleen, skeletal muscle, gill, and brain, and the expression level in the skeletal muscle was extremely significantly higher than in other examined tissues. Tbmstn2 was expressed in the skin, skeletal muscle, gill, and brain, and had the highest expression in the skeletal muscle, followed by expression in the brain. Meanwhile, in different stages of embryonic development, the expression of Tbmstn1 started from the gastrula stage. Its expression in the eye-pigment formation stage and hatching stage was significantly higher than that in other stages. The Tbmstn2 was expressed in all examined embryonic stages with different levels, and the highest expression was detected in the eye-pigment formation stage. These results suggested that Tbmstn1 and Tbmstn2 may involve in the development of skeletal muscle, and Tbmstn2 may be related to the formation of nervous system.

scholarly journals 343 Wnt/β-catenin pathway is required for porcine satellite cell proliferation and differentiation to promote skeletal muscle growth

2019 ◽  
Vol 97 (Supplement_3) ◽  
pp. 97-97
Author(s):  
Zong-ming Zhang ◽  
Chun-qi Gao ◽  
Hui-chao Yan ◽  
Xiu-qi Wang
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Satellite Cell ◽  
Muscle Growth ◽  
Control Group ◽  
Skeletal Muscle Growth ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Deficiency Group

Abstract Wnt/β-catenin plays a crucial role in skeletal muscle growth, but its specific mechanism still unclear. In this study, due to the distinct role of lysine in pig industry, we provided it as an entry point to investigate the role of Wnt/β-catenin in governing skeletal muscle growth. Firstly, total 18 weaned piglets were divided into three groups: control group, lysine deficiency group and lysine re-supplementation group (lysine levels added from 0.83% to 1.31% at 14 d). After 28 d experiment, all pigs were slaughtered to measure the change of Wnt/β-catenin in skeletal muscle. Secondly, satellite cell (SC) was isolated and cultured with Wnt activator, such as Wnt3a and WRN (Wnt3a, R-spondin1, Noggin) after lysine deficiency for 48 h to investigate cell proliferation and differentiation ability and the level of Wnt/β-catenin in different conditions. The results showed that compared with the control group, lysine deficiency significantly reduced longissimus dorsi muscle weight and Pax7 positive SC, and inhibited Wnt/β-catenin (P < 0.05). Fortunately, these restrictions were rescued to the control levels by lysine re-supplementation (P > 0.05). Meanwhile, compared with the lysine deficiency group, the MTT and western blotting assay showed cell proliferation ability was significantly increased with re-activated Wnt/β-catenin by re-supplemented lysine, Wnt3a or WRN (P < 0.05), respectively. Moreover, under the condition of cell differentiation, compared with the control group, cell fusion index was significantly decreased in the lysine deficiency group (P < 0.05), whereas it was significantly increased with lysine re-supplementation group, Wnt3a or WRN respective supplementation group in comparison with the lysine deficiency group (P < 0.05). In addition, compared with the lysine deficiency group, the protein levels of myogenic regulatory factors and Wnt/β-catenin pathway were also re-activated by re-supplemented lysine, Wnt3a or WRN (P < 0.05). Collectively, we found Wnt/β-catenin activation is required for porcine SC proliferation and differentiation to promote skeletal muscle growth.

scholarly journals The Effects of Marine Algal Polyphenols, Phlorotannins, on Skeletal Muscle Growth in C2C12 Muscle Cells via Smad and IGF-1 Signaling Pathways

Marine Drugs ◽  
2021 ◽  
Vol 19 (5) ◽  
pp. 266
Author(s):  
Seo-Young Kim ◽  
Ji-Hyeok Lee ◽  
Nalae Kang ◽  
Kil-Nam Kim ◽  
You-Jin Jeon
Keyword(s):  
Skeletal Muscle ◽  
Muscle Growth ◽  
Negative Regulator ◽  
Growth Effect ◽  
C2c12 Myoblast ◽  
Synthetic Drugs ◽  
Proliferation And Differentiation ◽  
Myoblast Proliferation ◽  
C2c12 Muscle Cells ◽  
Marine Algal

Skeletal muscle is an important tissue in energy metabolism and athletic performance. The use of effective synthetic supplements and drugs to promote muscle growth is limited by various side effects. Moreover, their use is prohibited by anti-doping agencies; hence, natural alternatives are needed. Therefore, we evaluated the muscle growth effect of substances that can act like synthetic supplements from edible marine algae. First, we isolated six marine algal polyphenols belonging to the phlorotannin class, namely dieckol (DK), 2,7′′-phloroglucinol-6,6′-bieckol (PHB), phlorofucofuroeckol A (PFFA), 6,6′-bieckol (6,6-BK), pyrogallol-phloroglucinol-6,6′-bieckol (PPB), and phloroglucinol (PG) from an edible brown alga, Ecklonia cava and evaluated their effects on C2C12 myoblasts proliferation and differentiation. Of the six phlorotannin isolates evaluated, DK and PHB induced the highest degree of C2C12 myoblast proliferation. In addition, DK and PHB regulates myogenesis by down-regulating the Smad signaling, a negative regulator, and up-regulating the insulin-like growth factor-1 (IGF-1) signaling, a positive regulator. Interestingly, DK and PHB bind strongly to myostatin, which is an inhibitor of myoblast proliferation, while also binding to IGF-1 receptors. Moreover, they bind to IGF-1 receptor. These results suggest that DK and PHB are potential natural muscle building supplements and could be a safer alternative to synthetic drugs.

scholarly journals FGF-2–dependent signaling activated in aged human skeletal muscle promotes intramuscular adipogenesis

2021 ◽  
Vol 118 (37) ◽  
pp. e2021013118 ◽  
Author(s):  
Sebastian Mathes ◽  
Alexandra Fahrner ◽  
Umesh Ghoshdastider ◽  
Hannes A. Rüdiger ◽  
Michael Leunig ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Transcriptional Activation ◽  
Human Skeletal Muscle ◽  
Muscle Growth ◽  
Muscle Cells ◽  
Adeno Associated Virus ◽  
Adult Skeletal Muscle

Aged skeletal muscle is markedly affected by fatty muscle infiltration, and strategies to reduce the occurrence of intramuscular adipocytes are urgently needed. Here, we show that fibroblast growth factor-2 (FGF-2) not only stimulates muscle growth but also promotes intramuscular adipogenesis. Using multiple screening assays upstream and downstream of microRNA (miR)-29a signaling, we located the secreted protein and adipogenic inhibitor SPARC to an FGF-2 signaling pathway that is conserved between skeletal muscle cells from mice and humans and that is activated in skeletal muscle of aged mice and humans. FGF-2 induces the miR-29a/SPARC axis through transcriptional activation of FRA-1, which binds and activates an evolutionary conserved AP-1 site element proximal in the miR-29a promoter. Genetic deletions in muscle cells and adeno-associated virus–mediated overexpression of FGF-2 or SPARC in mouse skeletal muscle revealed that this axis regulates differentiation of fibro/adipogenic progenitors in vitro and intramuscular adipose tissue (IMAT) formation in vivo. Skeletal muscle from human donors aged >75 y versus <55 y showed activation of FGF-2–dependent signaling and increased IMAT. Thus, our data highlights a disparate role of FGF-2 in adult skeletal muscle and reveals a pathway to combat fat accumulation in aged human skeletal muscle.

Myostatin inhibits proliferation and insulin-stimulated glucose uptake in mouse liver cells

2014 ◽  
Vol 92 (3) ◽  
pp. 226-234 ◽  
Author(s):  
Rani Watts ◽  
Mostafa Ghozlan ◽  
Curtis C. Hughey ◽  
Virginia L. Johnsen ◽  
Jane Shearer ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Proliferation ◽  
Glucose Uptake ◽  
Liver Cell ◽  
Noncoding Rna ◽  
Muscle Growth ◽  
Liver Cells ◽  
Negative Regulator ◽  
Kinase Substrate ◽  
Akt Phosphorylation

Although myostatin functions primarily as a negative regulator of skeletal muscle growth and development, accumulating biological and epidemiological evidence indicates an important contributing role in liver disease. In this study, we demonstrate that myostatin suppresses the proliferation of mouse Hepa-1c1c7 murine-derived liver cells (50%; p < 0.001) in part by reducing the expression of the cyclins and cyclin-dependent kinases that elicit G1-S phase transition of the cell cycle (p < 0.001). Furthermore, real-time PCR-based quantification of the long noncoding RNA metastasis associated lung adenocarcinoma transcript 1 (Malat1), recently identified as a myostatin-responsive transcript in skeletal muscle, revealed a significant downregulation (25% and 50%, respectively; p < 0.05) in the livers of myostatin-treated mice and liver cells. The importance of Malat1 in liver cell proliferation was confirmed via arrested liver cell proliferation (p < 0.05) in response to partial Malat1 siRNA-mediated knockdown. Myostatin also significantly blunted insulin-stimulated glucose uptake and Akt phosphorylation in liver cells while increasing the phosphorylation of myristoylated alanine-rich C-kinase substrate (MARCKS), a protein that is essential for cancer cell proliferation and insulin-stimulated glucose transport. Together, these findings reveal a plausible mechanism by which circulating myostatin contributes to the diminished regenerative capacity of the liver and diseases characterized by liver insulin resistance.

MYOSTATIN - A MODERN UNDERSTANDING OF THE PHYSIOLOGICAL ROLE AND SIGNIFICANCE IN THE DEVELOPMENT OF AGE-ASSOCIATED DISEASES

2021 ◽  
pp. 701-706
Author(s):  
А.А. Газданова ◽  
В.Г. Кукес ◽  
О.К. Парфенова ◽  
Н.Г. Сидоров ◽  
А.В. Перков ◽  
...  
Keyword(s):  
Muscle Growth ◽  
Physiological Role ◽  
Review Article ◽  
Negative Regulator ◽  
Transforming Growth Factors ◽  
Endogenous Factors ◽  
Pathological Conditions ◽  
Physiological Properties ◽  
The Family

Миостатин - белок, принадлежащий к классу миокинов, семейству трансформирующих факторов роста β (TGF-β). В обзорной статье, анализирующей данные литературы, показана ключевая роль миостатина в развитии старческой саркопении и кахексии при различных патологических состояниях, таких как рак, ХСН, ХБП, ХОБЛ и др. В статье рассматривается структура миостатина, подробная схема синтеза и его активации, механизм действия как негативного регулятора роста и дифференцировки мышц при этих патологических состояниях. Выделены основные физиологические свойства и клиническое значение. Рассмотрены экзогенные и эндогенные факторы, регулирующие экспрессию миостатина, и возможные механизмы их действия. Myostatin is a protein belonging to the myokine class, the family of transforming growth factors β (TGF-β). The review article, based on the analysis of literature data, shows the key role of myostatin in the development of senile sarcopenia and cachexia in various pathological conditions, such as cancer, chronic heart failure, chronic renal failure, COPD, etc. The article discusses the structure of myostatin, provides a detailed diagram of the synthesis and activation of myostatin, the ways of implementing the mechanism of action as a negative regulator of muscle growth and differentiation in these pathological conditions. The main physiological properties and clinical significance are highlighted. Exogenous and endogenous factors regulating myostatin expression and possible mechanisms of their action are considered.

From skeletal muscle damage and regeneration to the hypertrophy induced by exercise: What is the role of different macrophages subsets?

2021 ◽  
Author(s):  
André Luis Araujo Minari ◽  
Ronaldo V. Thomatieli-Santos
Keyword(s):  
Skeletal Muscle ◽  
Muscle Damage ◽  
Muscle Adaptation ◽  
Muscle Recovery ◽  
Skeletal Muscle Damage ◽  
Know How ◽  
Tissue Healing ◽  
Macrophage Subsets

Macrophages are one of the top players when considering immune cells involved with tissue homeostasis. Recently, increasing evidence has demonstrated that these macrophages could also present two major subsets during tissue healing; proliferative macrophages (M1-like), which are responsible for increasing myogenic cell proliferation, and restorative macrophages (M2-like), which are accountable for the end of the mature muscle myogenesis. The participation and characterization of these macrophage subsets is critical during myogenesis, not only to understand the inflammatory role of macrophages during muscle recovery but also to create supportive strategies that can improve mass muscle maintenance. Indeed, most of our knowledge about macrophage subsets comes from skeletal muscle damage protocols, and we still do not know how these subsets can contribute to skeletal muscle adaptation. This narrative review aims to collect and discuss studies demonstrating the involvement of different macrophage subsets during the skeletal muscle damage/regeneration process, showcasing an essential role of these macrophage subsets during muscle adaptation induced by acute and chronic exercise programs.

scholarly journals MiR-34b-5p Mediates the Proliferation and Differentiation of Myoblasts by Targeting IGFBP2

Cells ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 360 ◽  
Author(s):  
Wang ◽  
Zhang ◽  
Li ◽  
Abdalla ◽  
Chen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Cell Cycle Progression ◽  
Muscle Development ◽  
Muscle Growth ◽  
Flow Cytometric Analysis ◽  
Luciferase Reporter ◽  
Cycle Progression ◽  
Flow Cytometric ◽  
Proliferation And Differentiation ◽  
Dual Luciferase Reporter Assay

As key post-transcriptional regulators, microRNAs (miRNAs) play an indispensable role in skeletal muscle development. Our previous study suggested that miR-34b-5p and IGFBP2 could have a potential role in skeletal muscle growth. Our goal in this study is to explore the function and regulatory mechanism of miR-34b-5p and IGFBP2 in myogenesis. In this study, the dual-luciferase reporter assay and Western blot analysis showed that IGFBP2 is a direct target of miR-34b-5p. Flow cytometric analysis and EdU assay showed that miR-34b-5p could repress the cell cycle progression of myoblasts, and miR-34b-5p could promote the formation of myotubes by promoting the expression of MyHC. On the contrary, the overexpression of IGFBP2 significantly facilitated the proliferation of myoblasts and hampered the formation of myotubes. Together, our results indicate that miR-34b-5p could mediate the proliferation and differentiation of myoblasts by targeting IGFBP2.

scholarly journals Skeletal muscle development in vertebrate animals

2015 ◽  
Vol 1 (2) ◽  
pp. 139-148
Author(s):  
Md Shahjahan
Keyword(s):  
Skeletal Muscle ◽  
Muscle Development ◽  
Muscle Fibers ◽  
Muscle Growth ◽  
Paraxial Mesoderm ◽  
Meat Production ◽  
Lineage Specification ◽  
Proliferation And Differentiation ◽  
Axial Musculature ◽  
Postnatal Stage

This review covers the pre- and post-natal development of skeletal muscle of vertebrate animals with cellular and molecular levels. The formation of skeletal muscle initiates from paraxial mesoderm during embryogenesis of individuals which develops somites and subsequently forms dermomyotome derived myotome to give rise axial musculature. This process (myogenesis) includes stem and progenitor cell maintenance, lineage specification, and terminal differentiation to form myofibrils consequent muscle fibers which control muscle mass and its multiplication. The main factors of muscle growth are proliferation and differentiation of myogenic cells in prenatal stage and also the growth of satellite cells at postnatal stage. There is no net increase in the number of muscle fibers in vertebrate animals after hatch or birth except fish. The development of muscle is characterized by hyperplasia and hypertrophy in prenatal and postnatal stages of individuals, respectively, through Wnt signalling pathway including environment, nutrition, sex, feed, growth and myogenic regulatory factors. Therefore further studies could elucidate new growth related genes, markers and factors to enhance meat production and enrich knowledge on muscle growth.Asian J. Med. Biol. Res. June 2015, 1(2): 139-148

scholarly journals miR-194-5p negatively regulates the proliferation and differentiation of rabbit skeletal muscle satellite cells

2020 ◽  
Author(s):  
Yu Shi ◽  
Xudong Mao ◽  
Mingcheng Cai ◽  
Shenqiang Hu ◽  
Xiulan Lai ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Satellite Cells ◽  
Mammalian Species ◽  
Muscle Growth ◽  
Luciferase Reporter ◽  
Stem Cell Population ◽  
Muscle Satellite Cells ◽  
Skeletal Muscle Satellite Cells ◽  
Proliferation And Differentiation

Abstract Skeletal muscle satellite cells (SMSCs), also known as a multipotential stem cell population, play a crucial role during muscle growth and regeneration. In recent years, numerous miRNAs have been associated with the proliferation and differentiation of SMSCs in a number of mammalian species; however, the regulatory mechanisms of miR-194-5p in rabbit SMSCs still remain scarce. In this study, miR-194-5p was first observed to be highly expressed in the rabbit leg muscle. Furthermore, both the mimics and inhibitor of miR-194-5p were used to explore its role in the proliferation and differentiation of rabbit SMSCs cultured in vitro. Results from both EdU and CCK8 assays showed that miR-194-5p inhibited the proliferation of SMSCs. Meanwhile, Mef2c was identified as a target gene of miR-194-5p based on the dual-luciferase reporter assay results. In addition, upregulation of miR-194-5p decreased the expression levels of Mef2c and MyoG during rabbit SMSCs differentiation on Days 3 and 7 of in vitro culture. Taken together, these data demonstrated that miR-194-5p negatively regulates the proliferation and differentiation of rabbit SMSCs by targeting Mef2c.

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