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PubMed2026

FOS Regulates Myogenic and Adipogenic Differentiation via Extracellular Matrix Signaling.

In the livestock industry, intramuscular fat deposition is a key factor influencing meat tenderness and flavor. Although FOS (Fos proto-oncogene, AP-1 transcription factor subunit) has been implicated in the regulation of cell proliferation and differentiation, its differential roles in myogenic and adipogenic regulation remain unclear. In this study, we revealed that FOS markedly enhanced myogenic differentiation while inhibiting adipogenic differentiation in muscle stem cells, indicating that it exerts distinct effects on muscle development and intramuscular fat deposition. Mechanistically, FOS modulated extracellular matrix signaling by regulating FAK and PXN phosphorylation, acting as a molecular regulator between the muscle and fat lineages. Furthermore, exon SNPs in FOS were associated with slaughter weight and backfat thickness, and the mutant genotypes weakened its antiadipogenic effect. Collectively, these findings suggest that FOS is an important regulator of myogenic and adipogenic differentiation and is a potential candidate gene for the genetic improvement of meat quality traits.

Animals↗
PubMed1989

Localization of nicotinic acetylcholine receptor alpha-subunit transcripts during myogenesis and motor endplate development in the chick.

In 15-d-old chick latissimi dorsi muscles, the nicotinic acetylcholine receptor (AChR) alpha-subunit mRNA is densely accumulated at the level of subsynaptic nuclei of the motor endplate (Fontaine et al., 1988). In this paper, using in situ hybridization with genomic probes, we further show that the expression of the AChR alpha-subunit gene in the embryo, revealed by the accumulation of mature mRNAs, starts in myotomal cells and persists during the first stages of muscle development in a majority of muscle nuclei. Subsequently, the distribution of AChR alpha-subunit mRNAs becomes restricted to the newly formed motor endplates as neuromuscular junctions develop. To assess the transcriptional activity of individual nuclei in developing muscles, a strictly intronic fragment of the AChR alpha-subunit gene was used to probe in situ the level of unspliced transcripts. AChR alpha-subunit unspliced transcripts accumulate around a large number of sarcoplasmic nuclei at embryonic day 11, but can no longer be detected at their level after embryonic day 16 in the embryo. A similar decrease in the accumulation of AChR alpha-subunit transcripts is observed between day 4 and day 6 in primary cultures of muscle cells. On the other hand, in vivo denervation and in vitro blocking of muscle electrical activity by the sodium channel blocker tetrodotoxin results in an increase in the labeling of muscle nuclei. Yet, only 6% of the muscle nuclei appear labeled by the strictly intronic probes after denervation. The possible significance of such heterogeneity of muscle nuclei during motor endplate formation in AChR gene expression is discussed.

Actins↗
PubMed1997

Myonuclear accretion is a major determinant of avian skeletal muscle growth.

The role of satellite cells and DNA unit size in determining skeletal muscle growth was studied after mitotic activity was inhibited in the left pectoralis thoracicus of 2-wk-old tom turkeys by means of a 25-Gy dose of irradiation. Toms were killed and muscle weights were obtained 1 (n = 5), 4 (n = 6), 7 (n = 6), and 15 (n = 4) wk after irradiation. Satellite cell mitotic activity and DNA unit size were determined using enzymatically isolated myofiber segments and image analysis. Irradiated and nonirradiated muscle weights increased (P < 0.01) between all ages examined, but irradiated muscle weights were significantly (P < 0.01) lower than nonirradiated muscle weights at 4, 7, and 15 wk after irradiation. Satellite cell mitotic activity was lower (P < 0.01) in irradiated than in nonirradiated muscles at 1 and 4 wk after irradiation and resulted in a significant reduction (P < 0.05) in the number of myofiber nuclei per millimeter at 4 and 7 wk after irradiation. Satellite cell mitotic activity was higher (P < 0.05) in irradiated than in nonirradiated muscles at 7 wk after irradiation, but at 15 wk after irradiation it had fallen to low levels in both muscles. There was no significant (P > 0.10) difference in DNA unit size between muscles at any time, but there was an age-related increase (P < 0.01) for both muscles. Irradiation reduced muscle growth through a transient reduction in myonuclear production at a critical time (3-6 wk of age) in posthatch skeletal muscle development. The age-related increase in DNA unit size was not accelerated to compensate for the reduction in myonuclear accretion. Thus it appears that muscle growth potential is governed mostly by myonuclear accretion and to a lesser extent by DNA unit size.

Animals↗
PubMed2003

A targeted deletion of the C-terminal end of titin, including the titin kinase domain, impairs myofibrillogenesis.

Titin is the largest protein known, and is essential for organising muscle sarcomeres. It has many domains with a variety of functions, and stretches from the Z-line to the M-line in the muscle sarcomere. Close to the M-line, titin contains a kinase domain, which is known to phosphorylate the Z-line protein telethonin in developing muscle (Mayans, O., van der Ven, P. F., Wilm, M., Mues, A., Young, P., Furst, D. O., Wilmanns, M. and Gautel, M. (1998) Nature 395, 863-869). This phosphorylation is thought to be important for initiating or regulating myofibrillogenesis. We used a gene-targeting approach in cultured myoblasts to truncate the titin gene so that the kinase domain and other domains downstream of the kinase were not expressed. We recovered cells in which one allele was targeted. We found that these cells expressed both the full-length and a truncated titin that was approximately 0.2 MDa smaller than the corresponding band from wild-type cells. Myofibrillogenesis in these cells was impaired, in that the myotubes were shorter, and the organisation of the muscle sarcomeres, M- and Z-lines was poorer than in wild-type cells. There was also an overall reduction in levels of titin and skeletal myosin expression. These results suggest that the activity of the titin kinase domain and downstream sequence are important in organising myofibrils both at the M- and the Z-line early in myofibrillogenesis.

Animals↗
PubMed2006

Avian stanniocalcin-2 is expressed in developing striated muscle and joints.

The glycoprotein hormone stanniocalcin (STC) has originally been described in the teleost kidney. Since then, STC homologs have been identified in various genomes including human, mouse, rat, Xenopus and zebrafish. In mammals, two STC genes, STC1 and STC2, are known. We cloned a chicken STC homolog to analyze its expression pattern during chick development. Sequence analyses revealed a high sequence similarity of the chicken STC (cSTC) clone to mammalian STC2. Interestingly the expression pattern of cSTC2 largely resembles those of murine STC1: we found expression of cSTC2 in the nephric tubules, in the myocardium, in skeletal muscle cells from the onset of differentiation, and in synovial joint anlagen of the limbs.

Amino Acid Sequence↗
PubMed2004

Development of the Muscle Dysmorphia Inventory (MDI).

AIM: The development of the 6-factor, 27-item Muscle Dysmorphia Inventory (MDI) was based on Lantz et al. proposed model of characteristics associated with Muscle Dysmorphia. METHODS EXPERIMENTAL DESIGN: quantitative procedures including item-to-total correlations, exploratory and confirmatory factor analyses, and structure equation modeling confirmed the construct validity of the scale. Convergent validity was also tested. SETTING: bodybuilding and powerlifting competition venues, weight training facilities, and university athletic venues. PARTICIPANTS: the 1(st) study consisted of 77 experienced male free weight lifters. The 2(nd) study consisted of 156 male non-competitive bodybuilders and weight lifters and 168 elite level powerlifters and bodybuilders. The 3(rd) study consisted of 151 male and female bodybuilders and weight lifters. MEASURES: each participant completed demographic information, the MDI, Drive for Thinness subscale of the Eating Disorder Inventory, and the Training Dependency subscale of the Bodybuilding Dependence Scale. RESULTS: Reliability estimates (Cronbach's a) ranged from 0.72 to 0.94. Factor loadings in all 3 studies supported the 6-factor structure (size/symmetry, supplement use, exercise dependence, pharmacological use, dietary behavior, and physique protection). Much of the scale validation was focused on construct validity, however, correlations with the MDI's subscales and the Training Dependency subscale of the Bodybuilding Dependence Scale and the Drive for Thinness subscale of the Eating Disorder Inventory provided evidence of convergent validity also. CONCLUSIONS: From these preliminary results, the MDI appears to contribute to the identification of a newly formed disorder by offering a multi-dimensional measure of factors related to Muscle Dysmorphia.

Adult↗
PubMed1989

The cytoskeleton of arterial smooth muscle cells during development, atheromatosis, and tissue culture.

Arterial smooth muscle cells (SMCs) assume cytoskeletal features of embryonic cells during human and experimental atheromatosis, as well as when placed in culture. The expression of alpha-smooth muscle (SM) actin can be used to monitor these changes. The synthesis of alpha-SM actin is decreased early after plating in cultured cells and early after endothelial lesion in animals. The amount of mRNA for alpha-SM actin is not affected in cultured cells, although it is drastically decreased in the carotid artery after endothelial injury. Heparin does not modify in vivo the early decrease of alpha-SM actin mRNA and synthesis, but, by inhibiting the entry of SMC into the S phase of the cell cycle, it produces an early reinduction of alpha-SM actin.

Animals↗
PubMed1993

Effect of calcium agonists, BAY K 8644 and CGP 28392, on guinea pig airway smooth muscle function during development.

Dihydropyridine calcium agonists affect airway smooth muscle function by modulating the voltage-dependent calcium channel. Two such agonists, BAY K 8644 and CGP 28392 increase airway smooth muscle tone in adult guinea pigs but their actions during ontogeny are unknown. We compared contractile responses of airway tissue from fetal, newborn and young adult guinea pigs to cumulative doses of both BAY K 8644 and CGP 28392 under isometric conditions in vitro. Responses were examined in the presence and absence of aspirin to determine if endogenous cyclooxygenase products modulated these effects. BAY K 8644 generated a contractile response in 85 of 86 tissues. Maximum contraction was greater in extrathoracic tracheas from newborns when compared to adults (P < .05). In fetuses and newborns, contraction overall was greater in the presence of aspirin; however, in adult airways cyclooxygenase blockade did not appear to have any effect (P < .05). In contrast, CGP 28392 produced no contraction in 14 of 19 tracheas (all ages combined) in the presence of aspirin; whereas, all 18 tracheas in the absence of aspirin contracted. Also, there were no significant differences in maximum response among these age groups or tissue types to CGP 28392. Increased sensitivity of tracheas in immature guinea pigs was observed for both drugs in the absence of aspirin.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1997

Expression of myotonic dystrophy protein kinase gene during in vivo and in vitro mouse myogenesis.

Myotonic dystrophy (DM) is an autosomal dominant neuromuscular disorder characterized by a great variability in its clinical manifestations. The mutational basis underlying DM consists of an unstable (CTG)n trinucleotide repeat in the 3' untranslated region of the myotonic dystrophy protein kinase gene (DMPK). Conflicting results on DMPK gene expression in congenitally affected infants (CDM) have been published. Moreover, the prominence of satellite cells seen in muscle of CDM infants supports the notion that the congenital form is associated with an arrest in muscle development and suggests a role for the DMPK gene during differentiation and maturation of muscle. In order to clarify these findings, a comparative study of DMPK and myogenic factor mRNA levels was performed in developing mouse muscle tissues and cultured muscle cells at different developmental stages. Results show that DMPK gene expression is upregulated at a late stage of muscular development. This upregulation does not seem to depend on a given muscle specific bHLH factor.

Animals↗
PubMed1995

Receptor tyrosine kinase specific for the skeletal muscle lineage: expression in embryonic muscle, at the neuromuscular junction, and after injury.

While a number of growth factors have been described that are highly specific for particular cell lineages, neither a factor nor a receptor uniquely specific to the skeletal muscle lineage has previously been described. Here we identify a receptor tyrosine kinase (RTK) specific to skeletal muscle, which we term "MuSK" for muscle-specific kinase. MuSK is expressed at low levels in proliferating myoblasts and is induced upon differentiation and fusion. In the embryo, it is specifically expressed in early myotomes and developing muscle. MuSK is then dramatically down-regulated in mature muscle, where it remains prominent only at the neuromuscular junction; MuSK is thus the only known RTK that localizes to the neuromuscular junction. Strikingly, MuSK expression is dramatically induced throughout the adult myofiber after denervation, block of electrical activity, or physical immobilization. In humans, MuSK maps to chromosome 9q31.3-32, which overlaps with the region reported to contain the Fukuyama muscular dystrophy mutation. Identification of MuSK introduces a novel receptor-factor system that seems sure to play an important and selective role in many aspects of skeletal muscle development and function.

Amino Acid Sequence↗
PubMed1995

Comparison of the foetal development of muscle in normal and double-muscled cattle.

Muscle differentiation was studied in foetal Semitendinosus muscle from normal cattle and those with the 'culard' gene of muscular hypertrophy sampled at 90, 130, 170 and 210 days of foetal life. The different fibre types were characterized by immunohistochemistry with antibodies specific to different isoforms of myosin heavy chains. The isoforms were separated by electrophoresis, identified by immunoblotting and quantified by ELISA. In double-muscled animals, there was a slower rate of differentiation in the first generation of cells, most markedly apparent at 90 days. At 130 days, differentiation was retarded mainly in the second generation, while at 170 days there was no longer any difference between the two animal types in the differentiation of first generation cells, which were totally slow in both. At the same stage however, type IIC fibres in double-muscled animals were much slower in appearing and continued to be so at 210 days, albeit to a lesser extent. These findings show that differentiation of the muscle fibres occurs at a slower rate in double-muscled foetuses particularly during the first two-thirds of foetal life.

Animals↗
PubMed1983

Carcinoma in situ of the urinary bladder with and without associated vesical neoplasms.

Of 99 patients who had carcinoma-in situ (TIS) at least once between 1970 and 1980, 84 were subjected to detailed analysis and pathologic review. They may be classified into four groups: (Group 1) 14 patients, who presented with invasive bladder carcinoma (TCC) associated with TIS; (Group 2) 15 patients who, subsequent to the diagnosis of TIS with or without another superficial TCC developed muscle invasion (12 patients) or metastases without muscle invasion (three patients); (Group 3) 29 patients who underwent cystectomy for superficial TCC (Ta or T1, or TIS alone). Twenty (69%) had extravesical superficial extension. Two patients developed metastases subsequent to undergoing cystectomy; and (Group 4) 26 patients with TIS proven at least once who have not developed muscle invasion, metastases nor have undergone cystectomy. Nineteen had previous non-TIS superficial TCC. All patients in Groups 2 and 4 were treated conservatively (TUR +/- intravesical chemotherapy) when the initial diagnosis of TIS was made. Twelve patients in Group 3 underwent cystectomy within a month of the diagnosis of TIS. When 38 patients found to have TIS in association with the first diagnosis of superficial transitional cell carcinoma of the bladder were compared with 32 patients who had TIS diagnosed subsequent to their initial diagnosis of transitional cell carcinoma, the former group fared significantly worse (P less than 0.01) in regard to muscle invasion, metastases, or clinical indications for cystectomy.

Aged↗