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Leptin Stimulates the Synthesis of VEGF and activation of MAPK pathway in Cultured Mouse podocyte 원문보기

  • 저자

    지이화

  • 학위수여기관

    高麗大學校 大學院

  • 학위구분

    국내박사

  • 학과

    분자 인체 유전학과

  • 지도교수

  • 발행년도

    2004

  • 총페이지

    iv, 28p.

  • 키워드

    Mouse podocyte VEGF Leptin Stimulates MAAPK pathway;

  • 언어

    eng

  • 원문 URL

    http://www.riss.kr/link?id=T10068057&outLink=K  

  • 초록

    Background. Leptin, a small peptide hormone that is mainly produced in adipose tissue, inhibits food intake and increases energy expenditure. The kidney expresses abundant transcripts of the short form of leptin receptor (Ob-Ra), but the role of this hormone in podocyte is unknown. We examined the effects of leptin on the VEGF mRNA expression and protein production, which is one of the major pathogenic factors of diabetic nephropathy, in cultured mouse podocyte, and evaluated whether VEGF production depends on MAPK pathway. Methods. We treated leptin(1, 10, and 100nM) in cultured podocyte and harvested at 6, 24 and 72 hours to investigate the effects of leptin on the expression of VEGF mRNA and protein . In order to explore whether increased VEGF production by leptin depends on the p38 mitogen activated protein kinase (MAPK) or ERK pathway, we investigated the expressions of p38 MAPK and ERK mRNA and protein in response to the different concentrations of leptin (1, 10 and 100nM) in several time intervals (30 minutes, 1, 3, 6, 12 and 24hours). Furthermore, involvement of ERK pathway in the VEGF synthesis was also investigated by the prior treatment of PD98059, a specific ERK inhibitor. Results & Discussions. Only 100 nM of leptin increased the VEGF expression after 24 hours of incubation and this increment was observed until 72 hours. Leptin activated ERK signaling pathway and it was dependent on the rapid phosphorylation of p42/44 MAPK. However, ERK inhibitor (PD98059) did not diminish the stimulatory effect of leptin on the VEGF protein production Although leptin activated ERK pathway and increased VEGF synthesis, VEGF production induced by leptin did not show through the ERK pathway as a whole. Further studies will be needed to clarify the underlying mechanisms in leptin induced VEGF overproduction and to verify the pathophysiological implication of leptin in the development of diabetic nephropathy.


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