• Biomedical Science Letters
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• v.17 no.4
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• pp.283-289
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• 2011

Our previous study demonstrated that the Korean traditional medicine Gyeongshingangjeehwan (GGEx) activates AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) critical for fatty acid oxidation in skeletal muscle and C2C12 skeletal muscle cells. Thus, we examined whether GGEx can reduce lipid accumulation in these cells and tissues. After obese and type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats were treated with GGEx, we studied the effects of GGEx on skeletal muscle lipid accumulation. The effects of GGEx and/or the AMPK inhibitor compound C on lipid accumulation and expression of AMPK and $PPAR{\alpha}$ were measured in C2C12 skeletal muscle cells. Compared with lean Long-Evans Tokushima Otsuka rats, obese OLETF rats had increased triglyceride droplets. However, administration of GGEx to OLETF rats for 8 weeks significantly decreased triglyceride droplets in skeletal muscle. Consistent with the $in$ $vivo$ data, GGEx inhibited lipid accumulation, the degree of which was comparable to Wy14,643, the potent activator of $PPAR{\alpha}$. GGEx also increased skeletal muscle mRNA levels of AMPK${\alpha}1$, AMPK${\alpha}2$, and $PPAR{\alpha}$. However, compound C inhibited these effects in C2C12 cells. These results suggest that GGEx suppresses skeletal muscle lipid accumulation and this process may be mediated by AMPK and $PPAR{\alpha}$ activation.

• Food Science of Animal Resources
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• v.40 no.5
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• pp.852-859
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• 2020

The muscle stem cells of domestic animals are of interest to researchers in the food and biotechnology industries for the production of cultured meat. For producing cultured meat, it is crucial for muscle stem cells to be efficiently isolated and stably maintained in vitro on a large scale. In the present study, we aimed to optimize the method for the enrichment of pig muscle stem cells using a magnetic-activated cell sorting (MACS) system. Pig muscle stem cells were collected from the biceps femoris muscles of 14 d-old pigs of three breeds [Landrace×Yorkshire×Duroc (LYD), Berkshire, and Korean native pigs] and cultured in skeletal muscle growth medium-2 (SkGM-2) supplemented with epidermal growth factor (EGF), dexamethasone, and a p38 inhibitor (SB203580). Approximately 30% of total cultured cells were nonmyogenic cells in the absence of purification in our system, as determined by immunostaining for cluster of differentiation 56 (CD56) and CD29, which are known markers of muscle stem cells. Interestingly, following MACS isolation using the CD29 antibody, the proportion of CD56⁺/CD29⁺ muscle stem cells was significantly increased (91.5±2.40%), and the proportion of CD56 single-positive nonmyogenic cells was dramatically decreased. Furthermore, we verified that this method worked well for purifying muscle stem cells in the three pig breeds. Accordingly, we found that CD29 is a valuable candidate among the various marker genes for the isolation of pig muscle stem cells and developed a simple sorting method based on a single antibody to this protein.

• Journal of Yeungnam Medical Science
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• v.27 no.2
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• pp.91-97
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• 2010

Endothelial cells play a key role in pathological processes such as cancer cell metastasis, atherosclerosis, and diabetic retinopathy. Vascular smooth muscle cells directly involve in the formation of atheroma in atherosclerosis. Some kinds of the endothelial cells are simply harvested from the umbilical veins, the tunica intima of aortic walls, the retina using various enzymes solutions. Those purely isolated cells provide a powerful tool in vitro studies of the endothelial cell related diseases. In this context, the cultured smooth muscle cells after the isolation from the tunica media of aortic walls are also used for elucidating the pathogenesis of atherosclerosis. Here, I briefly introduce articles that include the isolation of human umbilical vein endothelial cells(HUVEC), aortic endothelial and smooth muscle cells, retinal microvascular endothelial cells(RMEC), as well as the diseases' applications of these cells.

• Applied Microscopy
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• v.27 no.1
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• pp.1-12
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• 1997

Dorsal and ventral epithelium of leech, Whitemenia edentula, were observed, using both light and electron-microscope. Results are as follows. Epithelia are composed of simple columnar or irregularly-shaped epithelium, the transveral folds were seen in the cross-sectioned dorsal and ventral epithelia, but only longitudinal folds(depth $500{\mu}m$, width $350{\mu}m$) were discovered in the ventral epithelium. As to muscular tissue under the dorsal epithelium of Whitemenia edentula, that of longitudinal muscle layer is thicker and more developed than that of circular muscle layer. Seven gland cells (type-A, B, C, D, E, F and H cells) and one pigment cell (type-G cell) were discovered in the whitemenia edentula. Those were identified as three kinds of the neutral mucopolysaccharide granoles (type-A, B and F cells), two kinds of acidic mucopolysaccharide granules (type-C and D cells), and two kinds of non-reactive granules respectively (type-E and F cells). The glanules of the type-A and type-B gland cells ae electronly high-dense, and surrounded by the muscular tissue. As to the distribution of gland cells, the type-A, type-B, type-C, type-D, type-I and type-H gland cells were discovered only between the connective tissue and the circular muscle layer, while type-F gland cells were discovered only between tile circular muscle layer and the longitudinal muscle layer.

• Journal of Life Science
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• v.12 no.2
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• pp.57-60
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• 2002

Apoptosis of vascular smooth muscle cell is observed in the vascular diseases such as atherosclerosis and restenosis. The death of vascular smooth muscle cells can be induced by cytokines and activation of Fas-pathways. It is widely accepted that apoptosis occurs without inflammation. There are, however, reports that apoptosis is not silent. Vascular smooth muscle cells dying by Fas-pathway secreted inflammatory cytokines including monocyte chemoattractant protein-1. This study have investigated whether apoptosis is associated with potent inflammatory cytokine tumor tumor necrosis factor (TNF)-${\alpha}$. The cells which undergo apoptosis by expressing FADD in the absence of tetracycline expressed and secreted TNF-${\alpha}$. When the level of TNF-${\alpha}$ transcript was investigated, dying smooth muscle cells exhibited transcriptional activation of TNF-${\alpha}$. The data indicate that dying vascular smooth muscle cells contribute to inflammation by expressing inflammatory cytokines. The present study suggests that apoptosis could not be silent in certain pathological situations.

• Korean Journal of Exercise Nutrition
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• v.23 no.2
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• pp.28-33
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• 2019

[Purpose] Recent studies have shown that glucose-6-phosphate isomerase (GPI)-which is a glycolysis interconversion enzyme-reduces oxidative stress. However, these studies are limited to tumors such as fibrosarcoma, and there are no studies that have examined the effects of exercise on GPI expression in mice skeletal muscle. Furthermore, GPI acts in an autocrine manner thorough its receptor, autocrine motility factor receptor (AMFR); therefore, we investigated expression level changes of secreted GPI from skeletal muscle in in vitro study to examine the potential role of GPI on skeletal muscle. [Methods] First, we performed an in vitro study, to identify the condition that upregulates GPI levels in skeletal muscle cells; we treated C2C12 muscle cells with an exercise-mimicking chemical, AICAR. AICAR treatment upregulated GPI expression level in C2C12 cell and its secretomes. To confirm the direct effect of GPI on skeletal muscle cells, we treated C2C12 cells with GPI recombinant protein. [Results] We found that GPI improved the viability of C2C12 cells. In the in vivo study, the exercise-treated mice group showed upregulated GPI expression in skeletal muscle. Based on the in vitro study results, we speculated that expression level of GPI in skeletal muscle might be associated with muscle function. We analyzed the association between GPI expression level and the grip strength of the all mice group. The mice group's grip strengths were upregulated after 2 weeks of treadmill exercise, and GPI expression level positively correlated with the grip strength. [Conclusion] These results suggested that the exercise-induced GPI expression in skeletal muscle might have a positive effect on skeletal muscle function.

• Textile Coloration and Finishing
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• v.34 no.4
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• pp.284-301
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• 2022

The limitations of food production caused by global warming, consumption of soil fertility, and land shortage have demanded the development of alternative foods. Their market has been increasing, and in particular, there is an urgent need for an alternative meat. Among them, the non-slaughtered cell-cultured meat that can be manufactured in the laboratory, that is, cultured meat, is in the spotlight, which can solve the problem of meat consumption while including the advantages of meat. It is classified into minced cultured meat and structured one with a structure similar to that of real meat. The latter is currently facing limitations related scaffolds, cells, and the multiplicative problems, and many attempts are being made to solve them. The complex problem is related to secure texture and taste as well as structural similarity to actual meat. To solve the problems, it is necessary to lay emphasis on cells, there are fat cells and vascular cells, and the most fundamental cells, muscle cells. These are the main cells that control the texture and nutrients of meat, and unlike other cells, they grow in the form of fibers. A myofibril (also known as a muscle fibril) is a basic rod-like organelle of a muscle cell, which is a quantitatively major component of meat, and one of the tissues that maintain the appearance of the body and bones. In this review article, we focused on the growth of muscle cells into long, tubular cells known as muscle fibers using the fabricated fibrous scaffold, and reviewed not only research results for muscle tissue engineering but also various results in the related fields for the last five years.

• Archives of Pharmacal Research
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• v.27 no.3
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• pp.324-333
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• 2004

To determine whether Insulin-like growth factor (IGF-I) treatment represents a potential means of enhancing the survival of cardiac muscle cells from adriamycin (ADR)-induced cell death, the present study examined the ability of IGF-I to prevent cell death. The study was performed utilising the embryonic, rat, cardiac muscle cell line, H9C2. Incubating cardiac muscle cells in the presence of adriamycin increased cell death, as determined by MTT assay and annexin V-positive cell number. The addition of 100 ng/mL IGF-I, in the presence of adriamycin, decreased apoptosis. The effect of IGF-I on phosphorylation of PI, a substrate of phosphatidylinositol 3-kinase (PI 3-kinase) or protein kinase B (AKT), was also examined in H9C2 cardiac muscle cells. IGF-I increased the phosphorylation of ERK 1 and 2 and $PKC{\;}{\zeta}{\;}kinase$. The use of inhibitors of PI 3-kinase (LY 294002), in the cell death assay, demonstrated partial abrogation of the protective effect of IGF-I. The MEK1 inhibitor-PD098059 and the PKC inhibitor-chelerythrine exhibited no effect on IGF-1-induced cell protection. In the regulatory subunit of PI3K-p85- dominant, negative plasmid-transfected cells, the IGF-1-induced protective effect was reversed. This data demonstrates that IGF-I protects cardiac muscle cells from ADR-induced cell death. Although IGF-I activates several signaling pathways that contribute to its protective effect in other cell types, only activation of PI 3-kinase contributes to this effect in H9C2 cardiac muscle cells.

• Proceedings of the Korean Society of Veterinary Pathology Conference
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• 2002.11a
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• pp.144-144
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• 2002

Muscular lesion was detected in a 23-month-old castrated bull encountered at Kyungsan slaughter house. The lesion appeared as fat intervening muscle fibers. The affected animal had no clinical signs. On microscopic examination, there was replacement of many muscle fibers by normal fat cells. Numerous fat cells were located between muscle fibers. Remaining skeletal muscle cells were in degenerative process, and thus abnormal skeletal muscle cells had loose fibers while normal had intact ones. The advent of inflammatory cells is not at the lesion, which is unique view in steatosis.

• Food Science of Animal Resources
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• v.41 no.4
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• pp.623-635
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• 2021

The effect of deer antler extract on muscle differentiation and muscle atrophy were evaluated to minimize muscle loss following aging. Various deer antler extracts (HWE, hot water extract of deer antler; FE, HWE of fermented deer antler; ET, enzyme-assisted extract of deer antler; UE, extract prepared by ultrasonication of deer antler) were evaluated for their effect on muscle differentiation and inhibition of 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)-induced muscle atrophy in C2C12 cells. Morphological changes according to the effect of antler extracts on muscle differentiation were confirmed by Jenner-Giemsa staining. In addition, the expression levels of genes related to muscle differentiation and atrophy were confirmed through qRT-PCR. In the presence of antler extracts, the length and thickness of myotubes and myogenin differentiation 1 (MyoD1) and myogenic factor 5 (Myf5) gene expression were increased compared to those in the control group (CON). Gene expression of AMP-activated protein kinase (AMPK), MyoD1, and myogenin, along with the muscle atrophy factors muscle RING finger-1 (MuRF-1) and forkhead box O3a (FoxO3a) upon addition of deer antler extracts to muscle-atrophied C2C12 cells was determined by qRT-PCR after treatment with AICAR. The expression of MuRF-1 and FoxO3a decreased in the groups treated with antler extracts compared to that in the group treated with AICAR alone. In addition, gene expression of MyoD1 and myogenin in the muscle atrophy cell model was significantly increased compared that into the CON. Therefore, our findings indicate that antler extract can increase the expression of MyoD1, Myf5 and myogenin, inhibit muscle atrophy, and promote muscle differentiation.