• 제목/요약/키워드: Myogenic response

검색결과 16건 처리시간 0.017초

Myogenic Differentiation of p53- and Rb-deficient Immortalized and Transformed Bovine Fibroblasts in Response to MyoD

  • Jin, Xun;Lee, Joong-Seub;Kwak, Sungwook;Jung, Ji-Eun;Kim, Tae-Kyung;Xuo, Chenxiong;Hong, Zhongshan;Li, Zhehu;Kim, Sun-Myoung;Whang, Kwang Youn;Hong, Ki-Chang;You, Seungkwon;Choi, Yun-Jaie;Kim, Hyunggee
    • Molecules and Cells
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    • 제21권2호
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    • pp.206-212
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    • 2006
  • We have established in culture a spontaneously immortalized bovine embryonic fibroblast (BEF) cell line that has lost p53 and $p16^{INK4a}$ functions. MyoD is a muscle-specific regulator capable of inducing myogenesis in a number of cell types. When the BEF cells were transduced with MyoD they differentiated efficiently to desmin-positive myofibers in the presence of 2% horse serum and 1.7 nM insulin. The myogenic differentiation of this cell line was more rapid and obvious than that of C2C12 cells, as judged by morphological changes and expression of various muscle regulatory factors. To confirm that lack of the p53 and $p16^{INK4a}$ pathway does not prevent MyoD-mediated myogenesis, we established a cell line transformed with SV40LT (BEFV) and introduced MyoD into it. In the presence of 2% horse serum and 1.7 nM insulin, the MyoD-transduced BEFV cells differentiated like the MyoD-transduced BEFS cells, and displayed a similar pattern of expression of muscle regulatory proteins. Taken together, our results indicate that MyoD overexpression overcomes the defect in muscle differentiation associated with immortalization and cell transformation caused by the loss of p53 and Rb functions.

Effect of ciglitazone on adipogenic transdifferentiation of bovine skeletal muscle satellite cells

  • Zhang, Junfang;Li, Qiang;Yan, Yan;Sun, Bin;Wang, Ying;Tang, Lin;Wang, Enze;Yu Jia;Nogoy, Kim Margarette Corpuz;Li, Xiangzi;Choi, Seong-Ho
    • Journal of Animal Science and Technology
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    • 제63권4호
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    • pp.934-953
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    • 2021
  • Ciglitazone is a member of the thiazolidinedione family, and specifically binds to peroxisome proliferator-activated receptor-γ (PPARγ), thereby promoting adipocyte differentiation. We hypothesized that ciglitazone as a PPARγ ligand in the absence of an adipocyte differentiation cocktail would increase adiponectin and adipogenic gene expression in bovine satellite cells (BSC). Muscle-derived BSCs were isolated from six, 18-month-old Yanbian Yellow Cattle. The BSC were cultured for 96 h in differentiation medium containing 5 µM ciglitazone (CL), 10 µM ciglitazone (CM), or 20 µM ciglitazone (CH). Control (CON) BSC were cultured only in a differentiation medium (containing 2% horse serum). The presence of myogenin, desmin, and paired box 7 (Pax7) proteins was confirmed in the BSC by immunofluorescence staining. The CL, CM, and CH treatments produced higher concentrations of triacylglycerol and lipid droplet accumulation in myotubes than those of the CON treatment. Ciglitazone treatments significantly increased the relative expression of PPARγ, CCAAT/enhancer-binding protein alpha (C/EBPα), C/EBPβ, fatty acid synthase, stearoyl-CoA desaturase, and perilipin 2. Ciglitazone treatments increased gene expression of Pax3 and Pax7 and decreased expression of myogenic differentiation-1, myogenin, myogenic regulatory factor-5, and myogenin-4 (p < 0.01). Adiponectin concentration caused by ciglitazone treatments was significantly greater than CON (p < 0.01). RNA sequencing showed that 281 differentially expressed genes (DEGs) were found in the treatments of ciglitazone. DEGs gene ontology (GO) analysis showed that the top 10 GO enrichment significantly changed the biological processes such as protein trimerization, negative regulation of cell proliferation, adipocytes differentiation, and cellular response to external stimulus. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that DEGs were involved in the p53 signaling pathway, PPAR signaling pathway, biosynthesis of amino acids, tumor necrosis factor signaling pathway, non-alcoholic fatty liver disease, PI3K-Akt signaling pathway, and Wnt signaling pathway. These results indicate that ciglitazone acts as PPARγ agonist, effectively increases the adiponectin concentration and adipogenic gene expression, and stimulates the conversion of BSC to adipocyte-like cells in the absence of adipocyte differentiation cocktail.

장애환자에서 치성감염에 의한 아관긴급과 구강피부누공의 관리 (CARE OF TRISMUS AND OROCUTANEOUS FISTULA BY ODONTOGENIC INFECTION IN A DISABLED PATIENT)

  • 오지현;손정석;유재하;김종배
    • 대한장애인치과학회지
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    • 제9권2호
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    • pp.111-117
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    • 2013
  • Some odontogenic infections erode into fascial spaces directly and spread toward lymphatic tissues and blood streams. The principal maxillary primary spaces are the canine, buccal, and infratemporal space, the next secondary spaces are the masseteric, temporal and pharygeal space. As a result of the infection, trismus and orocutaneous fistula may be occurred. Trismus is owing to conditions not associated with temporomandibular joint itself and may be of myogenic, neurogenic, or psychogenic nature. Muscular trismus is due to infection adjacent to the elevator muscles of the jaw. The four principles of treatment of infection are as follows: (1) removal of the cause, (2) establishment of drainage, (3) institution of antibiotic therapy, and (4) provision of supportive care, including rest, nutrition and physiotherapy. Jaw physiotherapy is necessary to increase the amount of mouth opening and regain normal muscle tone. If proper care of odontogenic infection could be attained, the orocutaneous fistula will heal and close spontaneously by wound contraction mechanism of natural homeostatic response. This is a case report of the care of trismus and orocutaneous fistula due to fascial space abscess by advanced odontogenic infection in a physically disabled patient.

Chondrogenesis of Mesenchymal Stem Cell Derived form Canine Adipose Tissue

  • Lee, Byung-Joo;Wang, Soo-Geun;Seo, Cheol-Ju;Lee, Jin-Chun;Jung, Jin-Sup;Lee, Ryang-Hwa
    • 대한음성언어의학회:학술대회논문집
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    • 대한음성언어의학회 2003년도 제19회 학술대회
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    • pp.183-183
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    • 2003
  • Background and Objectives : Cartilage reconstruction is one of medical issue in otolaryngology. Tissue engineering is presently being utilized in part of cartilage repair. Sources of cells for tissue engineering are chondrocyte from mature cartilage and bone marrow mesenchymal stem cells that are able to differentiate into chondrocyte. Recent studies have shown that adipose tissue have mesenchymal stem cells which can differentiate into adipogenic, chondrogenic myogenic osteogenic cells and neural cell in vitro. In this study, we have examined chondrogenic potential of the canine adipose tissue-derived mesenchymal stem cell(ATSC). Materials and Methods : We harvested canine adipose tissue from inguinal area. ATSCs were enzymatically released from canine adipose tissue. Under appropriate culture conditions, ATSCs were induced to differentiate into the chondrocyte lineages using micromass culture technique. We used immunostain to type II collagen and toluidine blue stain to confirm chondrogenic differentiation of ATSCs. Results : We could isolate ATSCs from canine adipose tissue. ATSCs expressed CD29 and CD44 which are specific surface markers of mesenchymal stem cell. ATSCs differentiated into micromass that has positive response to immunostain of type II collagen and toluidine blue stain. Conclusion : In vitro, ATSCs differentiated into cells that have characteristic cartilage matrix molecules in the presence of lineage-specific induction factors. Adipose tissue may represent an alternative source to bone marrow-derived MSCs.

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Characterization of Tunicamycin as Anti-obesity Agent

  • Song, Ha-Suk;Kim, Hye-Min;Jung, Sook-Yung;Lee, Dong-Hee
    • Biomolecules & Therapeutics
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    • 제17권2호
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    • pp.162-167
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    • 2009
  • Adipocytes undergo adipocyte stress in the excessive presence of lipid. Adipocyte stress accompanies the typical signs of endoplasmic reticulum (ER) stress: unfolded protein response and overexpression of molecular chaperones. Apoptotic induction in adipocytes is known as a good strategy for treating obesity. The drug "tunicamycin" was tested for its therapeutic potential in inducing apoptosis on differentiating adipocytes of 3T3-L1. When the 3T3-L1 cells, stimulated for adipogenesis, were treated with tunicamycin, they showed typical ER stress symptoms. Despite progression in ER stress, however, the differentiated 3T3-L1 hardly proceeded to apoptosis based on the CHOP protein expression and FACS analysis. This is very different from C2C12, the myogenic counterpart of 3T3-L1, which showed significant apoptosis along with ER stress. This study also characterizes a potential mechanism whereby adipocyte may avoid apoptosis to sustain the pathological state of obesity. The level of GRP94 expression significantly upholds in 3T3-L1 under tunicamycin treatment compared to preadipocytes and C2C-12. When GRP94 expression was inhibited by siRNA, 3T3-L1 showed a higher level of CHOP expression compared to C2C12 cells. In conclusion, adipocytes exert an anti-apoptotic mechanism under ER stress caused by tunicamycin; thus, apoptotic induction in adipocyte is not a viable anti-obesity option. The unusual level of GRP94 may serve as a key role whereby adipocytes reach to the obesity level circumventing the apoptosis.

Ginsenoside Rg1 augments oxidative metabolism and anabolic response of skeletal muscle in mice

  • Jeong, Hyeon-Ju;So, Hyun-Kyung;Jo, Ayoung;Kim, Hye-Been;Lee, Sang-Jin;Bae, Gyu-Un;Kang, Jong-Sun
    • Journal of Ginseng Research
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    • 제43권3호
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    • pp.475-481
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    • 2019
  • Background: The ginsenoside Rg1 has been shown to exert various pharmacological activities with health benefits. Previously, we have reported that Rg1 promoted myogenic differentiation and myotube growth in C2C12 myoblasts. In this study, the in vivo effect of Rg1 on fiber-type composition and oxidative metabolism in skeletal muscle was examined. Methods: To examine the effect of Rg1 on skeletal muscle, 3-month-old mice were treated with Rg1 for 5 weeks. To assess muscle strength, grip strength tests were performed, and the lower hind limb muscles were harvested, followed by various detailed analysis, such as histological staining, immunoblotting, immunostaining, and real-time quantitative reverse transcription polymerase chain reaction. In addition, to verify the in vivo data, primary myoblasts isolated from mice were treated with Rg1, and the Rg1 effect on myotube growth was examined by immunoblotting and immunostaining analysis. Results: Rg1 treatment increased the expression of myosin heavy chain isoforms characteristic for both oxidative and glycolytic muscle fibers; increased myofiber sizes were accompanied by enhanced muscle strength. Rg1 treatment also enhanced oxidative muscle metabolism with elevated oxidative phosphorylation proteins. Furthermore, Rg1-treated muscles exhibited increased levels of anabolic S6 kinase signaling. Conclusion: Rg1 improves muscle functionality via enhancing muscle gene expression and oxidative muscle metabolism in mice.