• Asian-Australasian Journal of Animal Sciences
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• v.29 no.4
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• pp.479-486
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• 2016

A previous genome-wide association study (GWAS) exposed histone deacetylase 2 (HDAC2) as a possible candidate gene for breast muscle weight in chickens. The present research has examined the possible role of HDAC2 in skeletal muscle development in chickens. Gene expression was measured by quantitative polymerase chain reaction in breast and thigh muscles during both embryonic (four ages) and post-hatch (five ages) development and in cultures of primary myoblasts during both proliferation and differentiation. The expression of HDAC2 increased significantly across embryonic days (ED) in breast (ED 14, 16, 18, and 21) and thigh (ED 14 and 18, and ED 14 and 21) muscles suggesting that it possibly plays a role in myoblast hyperplasia in both breast and thigh muscles. Transcript abundance of HDAC2 identified significantly higher in fast growing muscle than slow growing in chickens at d 90 of age. Expression of HDAC2 during myoblast proliferation in vitro declined between 24 h and 48 h when expression of the marker gene paired box 7 (PAX7) increased and cell numbers increased throughout 72 h of culture. During induced differentiation of myoblasts to myotubes, the abundance of HDAC2 and the marker gene myogenic differentiation 1 (MYOD1), both increased significantly. Taken together, it is suggested that HDAC2 is most likely involved in a suppressive fashion in myoblast proliferation and may play a positive role in myoblast differentiation. The present results confirm the suggestion that HDAC2 is a functional gene for pre-hatch and post-hatch (fast growing muscle) development of chicken skeletal muscle.

• Journal of Animal Science and Technology
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• v.61 no.5
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• pp.260-271
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• 2019

The objective of this study was to determine the effect of different stocker management programs on skeletal muscle development and growth characteristics, satellite cell (SC) activity in growing-finishing beef cattle as well as the effects of SC-conditioned media on preadipocyte gene expression and differentiation. Fall-weaned Angus steers (n = 76; $258{\pm}28kg$) were randomly assigned to 1 of 4 stocker production systems: 1) grazing dormant native range (NR) supplemented with a 40% CP cottonseed meal-based supplement ($1.02kg{\cdot}steer^{-1}{\cdot}d^{-1}$) followed by long-season summer grazing (CON, 0.46 kg/d); 2) grazing dormant NR supplemented with a ground corn and soybean meal-based supplement fed at 1% of BW followed by short-season summer grazing (CORN, 0.61 kg/d); 3) grazing winter wheat pasture (WP) at high stocking density (3.21 steers/ha) to achieve a moderate rate of gain (LGWP, 0.83 kg/d); and 4) grazing winter WP at low stocking density (0.99 steers/ha) to achieve a high rate of gain (HGWP, 1.29 kg/d). At the end of the stocker (intermediate harvest, IH) and finishing (final harvest, FH) phases, 4 steers / treatment were harvested and longissimus muscles (LM) sampled for cryohistological immunofluorescence analysis and SC culture assays. At IH, WP steers had greater LM fiber cross-sectional area than NR steers; however, at FH, the opposite was observed (p < 0.0001). At IH, CORN steers had the lowest Myf-5+:Pax7+ SC density (p = 0.020), while LGWP steers had the most Pax7+ SC (p = 0.043). At FH, CON steers had the highest LM capillary density (p = 0.003) and their cultured SC differentiated more readily than all other treatments (p = 0.017). At FH, Pax7 mRNA was more abundant in 14 d-old SC cultures from HGWP cattle (p = 0.03). Preadipocytes exposed to culture media from proliferating SC cultures from WP cattle isolated at FH had more $PPAR{\gamma}$ (p = 0.037) and less FABP4 (p = 0.030) mRNA expression compared with NR cattle. These data suggest that different stocker management strategies can impact skeletal muscle growth, SC function, and potentially impact marbling development in growing-finishing beef cattle.

• Nutrition Research and Practice
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• v.18 no.4
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• pp.451-463
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• 2024

BACKGROUND/OBJECTIVES: The umami taste receptor (TAS1R1/TAS1R3) is endogenously expressed in skeletal muscle and is involved in myogenesis; however, there is a lack of evidence about whether the expression of the umami taste receptor is involved in muscular diseases. This study aimed to elucidate the effects of the umami taste receptor and its mechanism on muscle wasting in cancer cachexia using in vivo and in vitro models. MATERIALS/METHODS: The Lewis lung carcinoma-induced cancer cachexia model was used in vivo and in vitro, and the expressions of umami taste receptor and muscle atrophy-related markers, muscle atrophy F-box protein, and muscle RING-finger protein-1 were analyzed. RESULTS: Results showed that TAS1R1 was significantly downregulated in vivo and in vitro under the muscle wasting condition. Moreover, overexpression of TAS1R1 in vitro in the human primary cell model protected the cells from muscle atrophy, and knockdown of TAS1R1 using siRNA exacerbated muscle atrophy. CONCLUSION: Taken together, the umami taste receptor exerts protective effects on muscle-wasting conditions by restoring dysregulated muscle atrophy in cancer cachexia. In conclusion, this result provided evidence that the umami taste receptor exerts a therapeutic anti-cancer cachexia effect by restoring muscle atrophy.

• Anatomy and Cell Biology
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• v.56 no.1
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• pp.145-149
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• 2023

Agenesis or congenital hypoplasia of skeletal muscles occurs infrequently but may occur with specific conditions such as Poland syndrome. The trapezius muscle can vary in the extent of its bony attachments or may have additional slips, however congenital absence or hypoplasia is extremely rare. There are only a few reports of partial or complete absence of the trapezius muscle. Two cases of bilateral absence of the trapezius were both in males and were accompanied by the absence of additional muscle in the pectoral girdle. Herein, we describe a case of a 56-year-old male cadaver with bilateral hypoplasia of the trapezius. The muscle was largely represented by atrophied muscle fibers with an abundance of fibrotic or fatty connective tissue. This subject had very minor hypoplasia of the left pectoralis major muscle, but the remaining muscles of the pectoral girdle were normal. The spinal accessory nerve terminated in the sternocleidomastoid muscle on both sides, failing to reach the trapezius. We interpret these findings to be consistent with a minor variant of Poland syndrome.

• BMB Reports
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• v.55 no.2
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• pp.104-109
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• 2022

Skeletal myogenesis is essential to keep muscle mass and integrity, and impaired myogenesis is closely related to the etiology of muscle wasting. Recently, miR-141-3p has been shown to be induced under various conditions associated with muscle wasting, such as aging, oxidative stress, and mitochondrial dysfunction. However, the functional significance and mechanism of miR-141-3p in myogenic differentiation have not been explored to date. In this study, we investigated the roles of miR-141-3p on CFL2 expression, proliferation, and myogenic differentiation in C2C12 myoblasts. MiR-141-3p appeared to target the 3'UTR of CFL2 directly and suppressed the expression of CFL2, an essential factor for actin filament (F-actin) dynamics. Transfection of miR-141-3p mimic in myoblasts increased F-actin formation and augmented nuclear Yes-associated protein (YAP), a key component of mechanotransduction. Furthermore, miR-141-3p mimic increased myoblast proliferation and promoted cell cycle progression throughout the S and G2/M phases. Consequently, miR-141-3p mimic led to significant suppressions of myogenic factors expression, such as MyoD, MyoG, and MyHC, and hindered the myogenic differentiation of myoblasts. Thus, this study reveals the crucial role of miR-141-3p in myogenic differentiation via CFL2-YAP-mediated mechanotransduction and provides implications of miRNA-mediated myogenic regulation in skeletal muscle homeostasis.

• Journal of Life Science
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• v.22 no.4
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• pp.447-455
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• 2012

Akt plays an important role in a variety of cellular physiologies such as growth, proliferation, and differentiation. In skeletal muscle, Akt has been implicated in regulating regeneration, hypertrophy, and atrophy. In this study, the role of Akt has been examined during skeletal muscle differentiation. Culturing C2C12 myoblasts under low serum (1% horse serum) and high density converted cell morphology from a round shape to an elongated and multi-nucleated shape. Morphological changes were initiated from day 2 of differentiation. In addition, the expression of both myogenin G and myogenin D was elevated from day 2 of differentiation. Skeletal muscle differentiation was abolished by silencing Akt1 or Akt2, but was significantly enhanced by the over-expression of either Akt1 or Akt2. The activation of Akt was observed from day 2 of differentiation and disappeared after day 7. The expression of kruppel-like factor 4 was observed from day 6 of differentiation. Moreover, this expression was blocked in cells silencing either Akt1 or Akt2. In addition, the promoter activity of kruppel-like factor 4 was significantly reduced in cells silencing Akt1 or Akt2. These results suggest that Akt regulates skeletal muscle differentiation through the regulation of kruppel-like factor 4 expression.

• Journal of Korean Medicine Rehabilitation
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• v.18 no.1
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• pp.47-63
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• 2008

Objectives : Eucommiae cortex is reported that it helps bone and skeletal muscle stronger. In case of bone, many report is presented, but reports related to skeletal muscle are rarely existed. So in order to investigate effects of Eucommiae cortex on the skeletal muscle atrophy following stroke, cerebral infarct was induced by the middle cerebral artery occlusion (MCAO) in the rats. Methods : In order to induce MCAO rats, nylon suture was advanced and then blocked middle cerebral artery(MCA). Water extract of Eucommiae cortex was treated for 15 days, once a day orally, after the MCAO. Effects were evaluated with muscle weights, muscle fiber type composition, cross-sectioned area of muscle fibers in soleus and gastrocnemius of the unaffected and affected hind limbs. And MyoD protein expression in gastrocnemius was demonstrated with immunohistochemistry and western blotting. Results : In the affected hind limb of the MCAO rats, muscle weight loss of gastrocnemius and tibialis anterior muscles were attenuated by Eucommiae cortex treatment. In soleus muscle of the affected hind limb of the MCAO rats, increase of type-I fibers and decrease of type-II fibers were induced by Eucommiae cortex treatment. In soleus muscle of the affected hind limb of the MCAO rats, decrease of cross-sectioned areas of type-I fibers was attenuated by Eucommiae cortex treatment. In gastrocnemius muscle of the affected hind limb of the MCAO rats, increase of type-I fibers and decrease of type-II fibers were induced by Eucommiae cortex treatment. In gastrocnemius muscle of the affected hind limb of the MCAO rats, decreases of cross-sectioned areas of type-I and type-II fibers were attenuated by Eucommiae cortex treatment. In gastrocnemius muscle of the affected and unaffected hind limb of the MCAO rats, MyoD expressions were increased by Eucommiae cortex treatment. Conclusions : These results suggest that Eucommiae cortex has a protective effect against muscle atrophy, through the inhibition of the muscle cell apoptosis, following the central nervous system demage.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.5
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• pp.1356-1362
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• 2005

The purpose of this study os to investigative the effect of Carrageenan-Induced Pain on lower limb muscle and ligament of rat. To evaluate pain mechanism in muscle and ligament, pain was induced by the injection of 2% $0.1m{\ell}$ carrageenan into the left lower limb muscle of rats after rats were anesthesized with 3% enflurane. Rats were killed on 72 hours after pain induction under the anesthesia. anterior rectus femoris muscle and its ligament were removed from rat hind limb. Morphological changes of them were peformed by the observation of light and electron microscopes. In the light microscopic findings, the muscle cells were polyheadral and situated with each other without small gap in control group. nucleus of cell was seen along the cell margin, and muscle cell groups were divided by regular narrow gap in cross section. In the pain-induced group, muscle cell groups were divided each other by the irregular gap, and some of groups formed larger than other cell groups by the fusion. Intercellular gap of most cell groups were increased compared with control groups. And also, perimysium of muscle cell groups was swollen in cross section. In control group, muscle cells contacted each other closely and each cell was divided by perimysium. The intracellular gaps were not seen between myofibrills, and also striations were well defined between muscle cells in longitudinal section. In pain-induced group, muscle cells were divided by the small intracellular gaps. And also, muscle cell showed many a short cross or longitudinal intercellular gaps in longitudinal section. In light microscopic findings of control group, tendon was composed with many tendon fibers contacted each other closely without gap. The free margin of tendon was fused, and apso the tendon fibers did not invaded between muscles. In pain-induced group, tendon was divided small groups by intertendinous gap, and also the margin of tendon divided by small groups. In the free margin, tendon invaded into muscle cells, and also fibroblasts between tendon fibers were long and lance-shaped. From these results, it is suggested that pain induction by carrageenan injured rat skeletal muscle and ligament by the morphological changes.

• Journal of Animal Science and Technology
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• v.54 no.3
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• pp.219-226
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• 2012

Gender specificity in muscle growth and development is well known. Genesis of muscle is dependent on proliferation and differentiation potential of resident myogenic satellite cells (MSCs) present in muscle fibers. Multipotential capacity of forming myocyte, osteocyte, and adipocyte like cell makes MSCs a unique stem cell. To understand the molecular mechanism involved in determination of muscle quality due to difference in hormone concentration of different gender of animals, MSCs were isolated from bovine skeletal muscle and cultured in male, female, and castrated serum supplemented media. DNA microarray used consisted of 24,000 spots with 70 mer oligo in each spot. A total of 88 genes were up-regulated and 551 genes were down-regulated by more than two fold. Among up-regulated gene, 33, 34, and 21 genes were found up-regulated in cells grown in male, female, and castrated serum, respectively. Interestingly, male serum showed 4, female 11 and castrated male showed 4 genes expressed highly in each gender. Further study on the highly up-regulated gene may unfold the mystery of gender specificity found in muscle development. Also, the identification of differentially expressed genes in gender-specific serum will add information on infrastructure of bovine genome research.

• The Journal of Korean Physical Therapy
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• v.14 no.2
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• pp.1-15
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• 2002

Excitation-contraction coupling in skeletal muscle is process by which depolarization of the muscle fiber membrane, elicited by a nerve action potential, triggers the release of $Ca^{2+}$ from the sarcoplasmic reticulum(SR). The resulting rise in intracellular $Ca^{2+}$ concentration$([Ca^{2+}]_i)$ activates the troponin complex, thereby initiating the contraction of the muscle. The question remains as to what factors are involved in the inhibition of SR $Ca^{2+}$ release in fatigued muscle. The purpose of this study was determine whether ATP-sensitive $K^+(K_{ATP})$ channels are activated and contribute to decrease in $[Ca^{2+}]_i$ during fatigue development in the mouse skeletal muscle. To elucidate a role of $K_{ATP})$ in relation to ECC, I measured the modulation effects of $K_{ATP})$ channel blocker(glibenclamide) and opener(pinacidil) on $[Ca^{2+}]_i$ after fatiguing electrical field stimulation(FEFS). Intracellular $Ca^{2+}$ signals were recorded by conforcal laser microscopy(LSM 410) and monitored using the fluorescent $Ca^{2+}$-Sensitive indicator Fluo-3 AM. The results of this study were as followed: 1. The relative [Ca2'li after FEFS in the pre-glibenclamide-treated group was higher than the control. And relative $[Ca^{2+}]_i$ after FEFS in the pre-glibenclamide-treated group was lower than the control. 2. The relative $[Ca^{2+}]_i$ after FEFS for 3 min in the control, pre-glibenclamide-treated group and pre-pinacidil-treated group showed a similar pattern; the gradually significant decrease in $[Ca^{2+}]_i$. But, these decreasing pattern was most significant in the control. These findings suggest a tight relationship between $K_{ATP})$ and $Ca^{2+}$ in ECC during fatigue. Therefore, 1 thought that activation of $K_{ATP})$ channels may be one of mechanisms of the fatigue in skeletal muscle.