KOSEN 한인과학기술자네트워크

여러 논문이 있는데 다음 3 논문 참고 하시고 2번 논문은 원광대학교에서 했던 논문입니다. 류도곤 박사님 (063-850-6846, tkryu@wonkwang.ac.kr) 이 corresponding author로 되어있으니 참고하세요. 1. Mol Cell Biochem. 2006 Jan;281(1-2):163-71. Hyperglycemia induces apoptosis and p53 mobilization to mitochondria in RINm5F cells. Ortega-Camarillo C, Guzman-Grenfell AM, Garcia-Macedo R, Rosales-Torres AM, Avalos-Rodriguez A, Duran-Reyes G, Medina-Navarro R, Cruz M, Diaz-Flores M, Kumate J. Unidad de Investigacion Medica en Bioquimica, Hospital de Especialidades. CMNS XXI. Instituto Mexicano del Seguro Social, Mexico. The mechanisms related to hyperglycemia-induced pancreatic beta-cell apoptosis are poorly defined. Rat insulin-producing cells (RINm5F) cultured in high glucose concentrations (30 mM) showed increased apoptosis and protein p53 translocation to mitochondria. In addition, hyperglycemia induced both the disruption of mitochondrial membrane potential (Delta < eqid1 > (m)), and an increase in reactive oxygen species (ROS), as shown by fluorescence changes of JC-1 and dichlorodihydrofluorescein-diacetate (DCDHF-DA), respectively. The increased intracellular ROS by high glucose exposure was blunted by mitochondrial-function and NADPH-oxidase inhibitors. We postulate that the concomitant mobilization of p53 protein to the mitochondria and the subsequent changes on the Delta < eqid2 > (m), lead to an important pancreatic beta-cell apoptosis mechanism induced by oxidative stress caused by hyperglycemia. PMID: 16328969 [PubMed - in process] 2. Life Sci. 2005 Jan 7;76(8):917-29. Protective effect of Coptidis Rhizoma on S-nitroso-N-acetylpenicillamine (SNAP)-induced apoptosis and necrosis in pancreatic RINm5F cells. Kwon KB, Kim EK, Lim JG, Shin BC, Han SC, Song BK, Kim KS, Seo EA, Ryu DG. Department of Physiology, School of Oriental Medicine, Wonkwang University, Iksan, Chonbuk, 570-749, South Korea. Coptidis rhizoma (CR) is a herb used in many traditional prescriptions against diabetes mellitus in Asia for centuries. Our purpose was to determine the protective effect and its action mechanism of CR on the cytotoxicity of pancreatic beta-cells. Nitric oxide (NO) is believed to play a key role in the process of pancreatic beta-cell destruction leading to insulin-dependent diabetes mellitus (IDDM). Exposure of RINm5F cells to chemical NO donor such as S-nitroso-N-acetylpenicillamine (SNAP) induced apoptotic events such as the disruption of mitochondrial membrane potential (Deltapsim), cytochrome c release from mitochondria, activation of caspase-3, poly (ADP-ribose) polymerase cleavage and DNA fragmentation. Also, exposure of SNAP led to LDH release into medium, one of the necrotic events. However, pretreatment of RINm5F cells with CR extract protected both apoptosis and necrosis through the inhibition of Deltapsim disruption in SNAP-treated RINm5F cells. In addition, rat islets pretreated with CR extract retained the insulin-secretion capacity even after the treatment with IL-1beta. These results suggest that CR may be a candidate for a therapeutic or preventing agent against IDDM. PMID: 15589968 3.Apoptosis. 2004 Sep;9(5):599-607. Fatty acid protection from palmitic acid-induced apoptosis is lost following PI3-kinase inhibition. Beeharry N, Chambers JA, Green IC. School of Pharmacy and Biomolecular Sciences, University of Brighton, Brighton, BN2 4GJ East Sussex, UK. n.beeharry@brighton.ac.uk We have previously shown that saturated fatty acids induce DNA damage and cause apoptotic cell death in insulin-producing beta-cells. Here we examine further the effects of single or combined dietary fatty acids on RINm5F survival or cell death signalling. Palmitate and stearate, but not linoleate, oleate or palmitoylmethyl ester, induced growth inhibition and increased apoptosis in RINm5F cells following 24 h exposure. Co-incubation with inhibitors of ceramide synthesis, myriocin or fumonisin B(1), did not improve viability of palmitic acid treated RINm5F cells. The inhibitor of inducible nitric oxide synthase, 1400 W, similarly had no protective effect. However, linoleic acid protected against palmitic acid-induced apoptotic and necrotic cell death. The specific pharmacological inhibitors of phosphatidylinositol 3-kinase, LY294002 and wortmannin, abolished the protective effect of linoleic acid on apoptosis but not on necrosis. These data show that the growth inhibitory and apoptosis-inducing effect of the saturated fatty acid palmitate on RINm5F cells is prevented by co-incubation with the polyunsaturated fatty acid linoleate but not inhibitors of ceramide or nitric oxide generation. A key role for phosphatidylinositol 3-kinase in mediating the linoleic-acid reduction in apoptosis is suggested. PMID: 15314288

Roche에서 발간된 apoptosis 분석에 대해서 잘 정리한 매뉴얼이 있습니다. 첨부파일을 참고해 보세요. >RINm5F cell line을 이용한 Apoptosis 분석 kit 추천좀해주세요.. >그리고..여러다른목적의 분석 kit 또는 관련 논문이나 website를 알려주시면 감사하겠습니다.. >처음 cell culture를 하기에 상세하고 폭넓은 자료 부탁드립니다. >