http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
간암세포에서 저산소증에 의해 유도되는 VEGF의 발현기작에 대한 연구
권유욱,배수경,김정애,김규원,박병채 부산대학교 유전공학연구소 1997 분자생물학 연구보 Vol.13 No.-
Purpose: Hepatocellular carcinoma(HCC),a typical hypervasculized tumor is very sensitive to hypoxia and vascular endothelial growth factor(VEGF) has previously been identified to be up-regulated in response to hypoxia in several cell types. However, the molecular mechanisma by which hypoxia is sensed by the cells remain enigmatic. To investigate whether calcium and AP-1 are involved in hypoxia-sensing mechanism, we performed following eaperiments. Materials and Methods: Hep3B cells were grown in hypoxia condition. To assess cell viability, MTT assay was performed. To investigate the effect of calcium and AP-1,northern blot analysis was performed after treatment with BAPTA/AM. Results: The expression of VEGF was significantly up-regulated by hypoxia in Hep3B, hepatocellular carcinoma cell line. The increased expression of VEGF induced by hypoxia was blocked by the addition of BAPTA/AM, a cytosolic calcium chelator to the media. In addition, we found that the expression of c-jun protooncogene was also-regulated by hypoxia. Hypoxia increase of c-jun expression was also normalized by the treatment with BAPTA/AM. Conclusion: These results suggest that the increased expression of VEGF by hypoxia is mediated through the calcium and c-jun signalling pathway in the Hep3B human hepatoma cell lines.
간암세포에서 저산소증에 의해 유도되는 VEGF의 발현기작에 대한 연구
권유욱,배수경,김정애,김규원,박병채 영남대학교 약품개발연구소 1997 영남대학교 약품개발연구소 연구업적집 Vol.7 No.-
Puropse: Hepatocellular carcinoma (HCC), a typical hypervasculized tumor is very sensitive to hypoxia and vascular endothelial growth factor (VEGF) has previously been identified to be up-regulated in response to hypoxia in several cell types. However, the molecular mechanisms by which hypoxia is sensed by the cells remain enigmatic. To investigate whether calcium and AP-1 are involved in hypoxia-sensing mechanism, we performed following experiments. Materials and Methods: Hep3B cells were grown in hypoxic condition. To assess cell viability, MTT assay was performed. To investigate the effect of calcium and AP-1, northern blot analysis was performed after treatment with BAPTA/AM. Results: The expression of VEGF was significantly up-regulated by hypoxia in Hep3B, hepatocellular carcinoma cell line. The increased expression of VEGF induced by hypoxia was blocked by the addition of BAPTA/AM, a cytosolic calcium chelator to the media. In addition, we found that the expression of c-jun protooncogene was also up-regulated by hypoxia. Hypoxic increase of c-jun expression was also normalized by the treatment with BAPTA/AM. Conclusion: These results suggest that the increased expression of VEGF by hypoxia is mediated through the calcium and c-jun signalling pathway in the Hep3B human hepatoma cell lines.
Cell signaling and biological pathway in cardiovascular diseases
Cheong-Whan Chae,권유욱 대한약학회 2019 Archives of Pharmacal Research Vol.42 No.3
Currently, coronary artery disease accounts for a large proportion of deaths occurring worldwide. Damage to the heart muscle over a short period of time leads to myocardial infarction (MI). The biological mechanisms of atherosclerosis, one of the causes of MI, have been well studied. Resistin, a type of adipokine, is closely associated with intravascular level of low-density lipoprotein cholesterol and augmentation of the expression of adhesion molecules in endothelial cells. Therefore, resistin, which is highly associated with inflammation, can progress into coronary artery disease. Adenylyl cyclase associated protein 1, a binding partner of resistin, also plays an important role in inducing pro-inflammatory cytokines. The induction of these cytokines can aggravate atherosclerosis by promoting severe plaque rupture of the lesion site. Recently, drugs, such as statins that can inhibit inflammation have been extensively studied. The development of effective new drugs that can directly or indirectly block pro-inflammatory cytokines may have a great potential in the treatment of coronary artery disease in the future.