RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      KCI등재

      Effects of Insulin-Like Growth Factor-I on Expression of Suppressor of Cytokine Signaling-3 in C2C12 Myotube

      한글로보기

      https://www.riss.kr/link?id=A82722939

      • 0

        상세조회
      • 0

        다운로드
      서지정보 열기
      • 내보내기
      • 내책장담기
      • 공유하기
      • 오류접수

      부가정보

      국문 초록 (Abstract)

      SOCS-3와 IGF-I은 근육의 분화 과정 및 근비대 기전에 있어 매우 중요한 조절자 역할을 하는 유전자 및 성장인자이며, 최근 골격근에서 IGF-I과 SOCS-3 유전자의 상호작용에 관한 연구의 필요성이 제기되고 있다. 본 연구에서는 C2C12 myotube에서 IGF-I이 SOCS-3 유전자 발현에 미치는 영향에 대해 알아보기 위해 4일간 분화시킨 C2C12 myotube에 IGF-I을 다양한 농도(0-200 ng/ml) 및 시간(3-72 시간)에 따라 처리하였다. 그 결과 IGF-I이 SOCS-3 유전자의 단백질 발현을 시간 의존적으로 유의하게 증가시켰으며, 3 시간에서 mRNA 발현을 증가시키고, 시간이 지남에 따라 긴 시간에서는 농도 의존적으로 발현이 감소하였음을 알 수 있었다. 또한 면역형광 염색을 통해 IGF-I이 myotube에서 SOCS-3의 단백질을 발현시켰음을 뚜렷하게 관찰 할 수 있었다. 위 결과들을 바탕으로 본 연구에서는 IGF-I의 처리가 분화된 근육 세포인 C2C12 myotube에서 SOCS-3 유전자 발현에 유의한 영향을 미쳤음을 증명하였다. 이러한 결과는 선행연구에서 보고한 운동이 SOCS-3 유전자 발현을 증가시킴에 있어서 IGF-I이 중추적인 역할을 한 것으로 생각된다. 그러나 IGF-I에 의한 SOCS-3 유전자 발현 조절 기전에 있어 관련 신호 전달체계 및 골격근 관련 유전자 발현에 미치는 영향에 관한 연구는 보다 더 이루어져야 할 것이라 사료된다.
      번역하기

      SOCS-3와 IGF-I은 근육의 분화 과정 및 근비대 기전에 있어 매우 중요한 조절자 역할을 하는 유전자 및 성장인자이며, 최근 골격근에서 IGF-I과 SOCS-3 유전자의 상호작용에 관한 연구의 필요성이 ...

      SOCS-3와 IGF-I은 근육의 분화 과정 및 근비대 기전에 있어 매우 중요한 조절자 역할을 하는 유전자 및 성장인자이며, 최근 골격근에서 IGF-I과 SOCS-3 유전자의 상호작용에 관한 연구의 필요성이 제기되고 있다. 본 연구에서는 C2C12 myotube에서 IGF-I이 SOCS-3 유전자 발현에 미치는 영향에 대해 알아보기 위해 4일간 분화시킨 C2C12 myotube에 IGF-I을 다양한 농도(0-200 ng/ml) 및 시간(3-72 시간)에 따라 처리하였다. 그 결과 IGF-I이 SOCS-3 유전자의 단백질 발현을 시간 의존적으로 유의하게 증가시켰으며, 3 시간에서 mRNA 발현을 증가시키고, 시간이 지남에 따라 긴 시간에서는 농도 의존적으로 발현이 감소하였음을 알 수 있었다. 또한 면역형광 염색을 통해 IGF-I이 myotube에서 SOCS-3의 단백질을 발현시켰음을 뚜렷하게 관찰 할 수 있었다. 위 결과들을 바탕으로 본 연구에서는 IGF-I의 처리가 분화된 근육 세포인 C2C12 myotube에서 SOCS-3 유전자 발현에 유의한 영향을 미쳤음을 증명하였다. 이러한 결과는 선행연구에서 보고한 운동이 SOCS-3 유전자 발현을 증가시킴에 있어서 IGF-I이 중추적인 역할을 한 것으로 생각된다. 그러나 IGF-I에 의한 SOCS-3 유전자 발현 조절 기전에 있어 관련 신호 전달체계 및 골격근 관련 유전자 발현에 미치는 영향에 관한 연구는 보다 더 이루어져야 할 것이라 사료된다.

      더보기

      다국어 초록 (Multilingual Abstract)

      It is well known that both insulin-like growth factor-I and suppressor of cytokine signaling-3 (SOCS-3) are known to modulate various aspects of physiology in skeletal muscle cells. Furthermore, although SOCS-3 expression is related to insulin resistance in non-skeletal muscle cells and is known to interact with insulin-like growth factor-I receptor, the effect of IGF-I on SOCS-3 gene expression in skeletal muscle cells is presently unknown. C2C12 myotubes were treated with different concentrations (0-200 ng/ml) of IGF-I or for various periods of time (3-72 hr). Immunofluorescent staining image revealed that IGF-I induced SOCS-3 protein expression in a dose-dependent manner. Western blot data also showed that SOCS-3 proteins were induced by IGF-I (200 ng/ml) in C2C12 myotubes in a time-dependent manner. The level of SOCS-3 mRNA was also significantly increased after 3hr of IGF-I (10-100 ng/ml) treatment. However, the levels of SOCS-3 mRNA were significantly decreased after 24 and 48 hr of IGF-I (10-100 ng/ml) treatment compared to the control. In conclusion, SOCS-3 protein is induced by IGF-I treatment in C2C12 skeletal muscle cells and this induction is regulated pretranslationally. The modulating effect of IGF-I on SOCS-3 expression may be an important regulator of gene expression in skeletal muscle cells.
      번역하기

      It is well known that both insulin-like growth factor-I and suppressor of cytokine signaling-3 (SOCS-3) are known to modulate various aspects of physiology in skeletal muscle cells. Furthermore, although SOCS-3 expression is related to insulin resista...

      It is well known that both insulin-like growth factor-I and suppressor of cytokine signaling-3 (SOCS-3) are known to modulate various aspects of physiology in skeletal muscle cells. Furthermore, although SOCS-3 expression is related to insulin resistance in non-skeletal muscle cells and is known to interact with insulin-like growth factor-I receptor, the effect of IGF-I on SOCS-3 gene expression in skeletal muscle cells is presently unknown. C2C12 myotubes were treated with different concentrations (0-200 ng/ml) of IGF-I or for various periods of time (3-72 hr). Immunofluorescent staining image revealed that IGF-I induced SOCS-3 protein expression in a dose-dependent manner. Western blot data also showed that SOCS-3 proteins were induced by IGF-I (200 ng/ml) in C2C12 myotubes in a time-dependent manner. The level of SOCS-3 mRNA was also significantly increased after 3hr of IGF-I (10-100 ng/ml) treatment. However, the levels of SOCS-3 mRNA were significantly decreased after 24 and 48 hr of IGF-I (10-100 ng/ml) treatment compared to the control. In conclusion, SOCS-3 protein is induced by IGF-I treatment in C2C12 skeletal muscle cells and this induction is regulated pretranslationally. The modulating effect of IGF-I on SOCS-3 expression may be an important regulator of gene expression in skeletal muscle cells.

      더보기

      목차 (Table of Contents)

      • 서론
      • 재료 및 방법
      • 결과
      • 고찰
      • References
      • 서론
      • 재료 및 방법
      • 결과
      • 고찰
      • References
      • 초록
      더보기

      참고문헌 (Reference)

      1 Cacalano, N. A., "Tyrosine-phosphorylated SOCS-3 inhibits STAT activation but binds to p120 RasGAP and activates Ras" 3 : 460-465, 2001

      2 Alexander, W. S, "The role of suppressors of cytokine signaling (SOCS) proteins in regulation of the immune response" 22 : 503-529, 2004

      3 Shi, H., "Suppressor of cytokine signaling 3 is a physiological regulator of adipocyte insulin signaling" 279 : 34733-34740, 2004

      4 Rieusset, J., "Suppressor of cytokine signaling 3 expression and insulin resistance in skeletal muscle of obese and type 2 diabetic patients" 53 : 2232-2241, 2004

      5 Ueki, K., "Suppressor of cytokine signaling 1 (SOCS-1) and SOCS-3 cause insulin resistance through inhibition of tyrosine phosphorylation of insulin receptor substrate proteins by discrete mechanisms" 24 : 5434-5446, 2004

      6 Dey, B. R., "Suppressor of cytokine signaling (SOCS)-3 protein interacts with the insulin-like growth factor-I receptor" 278 : 38-43, 2000

      7 Glass, D. J, "Skeletal muscle hypertrophy and atrophy signaling pathways" 37 : 1974-1984, 2005

      8 Bodell, P. W., "Skeletal muscle growth in young rats is inhibited by chronic exposure to IL-6 but preserved by concurrent voluntary endurance exercise" 106 : 443-453, 2009

      9 Trenerry, M. K., "STAT3 signaling is activated in human skeletal muscle following acute resistance exercise" 102 : 1483-1489, 2007

      10 Takeda, K, "STAT family of transcription factors in cytokine-mediated biological responses" 11 : 199-207, 2000

      1 Cacalano, N. A., "Tyrosine-phosphorylated SOCS-3 inhibits STAT activation but binds to p120 RasGAP and activates Ras" 3 : 460-465, 2001

      2 Alexander, W. S, "The role of suppressors of cytokine signaling (SOCS) proteins in regulation of the immune response" 22 : 503-529, 2004

      3 Shi, H., "Suppressor of cytokine signaling 3 is a physiological regulator of adipocyte insulin signaling" 279 : 34733-34740, 2004

      4 Rieusset, J., "Suppressor of cytokine signaling 3 expression and insulin resistance in skeletal muscle of obese and type 2 diabetic patients" 53 : 2232-2241, 2004

      5 Ueki, K., "Suppressor of cytokine signaling 1 (SOCS-1) and SOCS-3 cause insulin resistance through inhibition of tyrosine phosphorylation of insulin receptor substrate proteins by discrete mechanisms" 24 : 5434-5446, 2004

      6 Dey, B. R., "Suppressor of cytokine signaling (SOCS)-3 protein interacts with the insulin-like growth factor-I receptor" 278 : 38-43, 2000

      7 Glass, D. J, "Skeletal muscle hypertrophy and atrophy signaling pathways" 37 : 1974-1984, 2005

      8 Bodell, P. W., "Skeletal muscle growth in young rats is inhibited by chronic exposure to IL-6 but preserved by concurrent voluntary endurance exercise" 106 : 443-453, 2009

      9 Trenerry, M. K., "STAT3 signaling is activated in human skeletal muscle following acute resistance exercise" 102 : 1483-1489, 2007

      10 Takeda, K, "STAT family of transcription factors in cytokine-mediated biological responses" 11 : 199-207, 2000

      11 Diao, Y., "SOCS1, SOCS3, and PIAS1 promote myogenic differentiation by inhibiting the leukemia inhibitory factor-induced JAK1/STAT1/STAT3 pathway" 29 : 5084-5093, 2009

      12 Emanuelli, B., "SOCS-3 is an insulin-induced negative regulator of insulin signaling" 275 : 15985-15991, 2000

      13 Emanuelli, B, "SOCS-3 inhibits insulin signaling and is up-regulated in response to tumor necrosis factor-alpha in the adipose tissue of obese mice" 276 : 47944-47949, 2001

      14 Spangenburg, E. E, "SOCS-3 induces myoblast differentiation" 280 : 10749-10758, 2005

      15 Rui, L., "SOCS-1 and SOCS-3 block insulin signaling by ubiquitin-mediated degradation of IRS1 and IRS2" 277 : 42394-42399, 2002

      16 Auernhammer, C. J., "SOCS proteins: modulators of neuroimmunoendocrine functions. Impact on corticotroph LIF signaling" 917 : 658-664, 2000

      17 Lebrun, P, "SOCS proteins causing trouble in insulin action" 192 : 29-36, 2008

      18 Jennische, E, "Regenerating skeletal muscle cells express insulin-like growth factor I" 130 : 327-332, 1987

      19 Hansen, J. A., "Mechanism of inhibition of growth hormone receptor signaling by suppressor of cytokine signaling proteins" 13 : 1832-1843, 1999

      20 Yadav, A., "JAK/STAT3 pathway is involved in survival of neurons in response to insulin-like growth factor and negatively regulated by suppressor of cytokine signaling-3" 280 : 31830-31840, 2005

      21 Wallenius, V., "Interleukin-6-deficient mice develop mature-onset obesity" 8 : 75-79, 2002

      22 Weigert, C., "Interleukin-6 acts as insulin sensitizer on glycogen synthesis in human skeletal muscle cells by phosphorylation of Ser473 of Akt" 289 : E251-257, 2005

      23 Benedetti, F., "Interleukin 6 causes growth impairment in transgenic mice through a decrease in insulin-like growth factor-I. A model for stunted growth in children with chronic inflammation" 99 : 643-650, 1997

      24 Park, P, "Insulin-like growth factor I (IGF-I) measurements in growth hormone (GH) therapy of idiopathic short stature (ISS)" 15 : S13-S20, 2005

      25 Sadowski, C. L., "Insulin Induction of SOCS-2 and SOCS-3 mRNA expression in C2C12 Skeletal Muscle Cells Is Mediated by Stat5" 276 : 20703-20710, 2001

      26 Haddad, F., "IL-6-induced skeletal muscle atrophy" 98 : 911-917, 2005

      27 Galvin, C. D., "IGF-I receptor mediates differentiation of primary cultures of mouse skeletal myoblasts" 200 : 19-29, 2003

      28 Yaspelkis, B. B. III., "High-fat feeding increases insulin receptor and IRS-1 coimmunoprecipitation with SOCS-3, IKKalpha/beta phosphorylation and decreases PI-3 kinase activity in muscle" 296 : R1709-R1715, 2009

      29 Nielsen, C., "Growth hormone signaling in vivo in human muscle and adipose tissue: impact of insulin, substrate background, and growth hormone receptor blockade" 93 : 2842-2850, 2008

      30 Tollet-Egnell, P., "Growth hormone regulation of SOCS-2, SOCS-3, and CIS messenger ribonucleic acid expression in the rat" 140 : 3693-3704, 1999

      31 Florini, J. R., "Growth hormone and the insulin-like growth factor system in myogenesis" 16 : 481-517, 1996

      32 Holloszy, J. O, "Exercise-induced increase in muscle insulin sensitivity" 99 : 338-343, 2005

      33 Hawley, J. A, "Exercise training-induced improvements in insulin action" 192 : 127-135, 2008

      34 Spangenburg, E. E, "Exercise increases SOCS-3 expression in rat skeletal muscle: potential relationship to IL-6 expression" 572 : 839-848, 2006

      35 Kim, C. H., "Effects of high-fat diet and exercise training on intracellular glucose metabolism in rats" 278 : E977-E984, 2000

      36 Kakisis, J. D., "Effects of cyclic strain on vascular cells" 11 : 17-28, 2004

      37 Jandziszak, K., "Disturbances of growth hormone-insulin-like growth factor axis and response to growth hormone in acidosis" 275 : R120-R128, 1998

      38 Ueki, K., "Central role of suppressors of cytokine signaling proteins in hepatic steatosis, insulin resistance, and the metabolic syndrome in the mouse" 10422-10427, 2004

      39 McLellan, A. S., "An E box in the exon 1 promoter regulates insulin-like growth factor-I expression in differentiating muscle cells" 291 : C300-C307, 2006

      40 Steppan, C. M., "Activation of SOCS-3 by resistin" 25 : 1569-1575, 2005

      41 Kraegen, E. W., "A potent in vivo effect of ciglitazone on muscle insulin resistance induced by high fat feeding of rats" 38 : 1089-1093, 1989

      더보기

      분석정보

      View

      상세정보조회

      0

      Usage

      원문다운로드

      0

      대출신청

      0

      복사신청

      0

      EDDS신청

      0

      동일 주제 내 활용도 TOP

      더보기

      주제

      연도별 연구동향

      연도별 활용동향

      연관논문

      연구자 네트워크맵

      공동연구자 (7)

      유사연구자 (20) 활용도상위20명

      인용정보 인용지수 설명보기

      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2027 평가예정 재인증평가 신청대상 (재인증)
      2021-01-01 평가 등재학술지 유지 (재인증) KCI등재
      2018-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2015-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2011-08-03 학술지명변경 외국어명 : Korean Journal of Life Science -> Journal of Life Science KCI등재
      2011-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2007-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2004-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2003-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2001-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
      더보기

      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.37 0.37 0.42
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.43 0.43 0.774 0.09
      더보기

      이 자료와 함께 이용한 RISS 자료

      나만을 위한 추천자료

      해외이동버튼