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정효균,이인규,강효경,서재미,김호,박기철,김동욱,김영근,오흥규,성민호 생화학분자생물학회 2002 Experimental and molecular medicine Vol.34 No.6
Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, known as statins, are widely used for primary and secondary prevention atherosclerosis is multistep processes where trans-endothelial migration of various leukocytes includ-ing monocytes is a crucial step. Interferon-γ (IFN-γ) contributes in this process by activating macro-phages and T-lymphocytes, and by inducing adhe-sion molecules in vascular endothelial and smooth muscle cells. In this study we investigated the expresion of intercellular cell adhesion mole-cule-1 (ICAM-1) in transformed endothelial cell line ECV304 cells as influenced by lovastatin, tumor necrosis factor-α (TNF-α) and IFN-γ. Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-γ-induced extracellular signal- regulated kinase (ERK) p44/p42-STAT1 signaling pathway. In cells treated with lovastatin and IFN-γ, ICAM-1 was expressed at a lower level than in cells treated with IFN-γ alone. However, lovastatin does not reduce TNF-α induced expression of ICAM-1. A similar result was observed in cells N-γ. Cis-acting DNA sequence elements were identified in the 5'-flanking region of the ICAM-1 promoter that mediate inhibition by lovastatin; these se-quences map to the IFN-γ activated site which also binds the STAT1 homodimer. However, lovastatin did not inhibit IFN-γ-mediated induction of the Y701 phosphorylated form of STAT1. But lovasta-tin does inhibit the IFN-γ-mediated phosphoryla-tion of ERK1/ERK2 (T202/Y204) and S727 phos-phorylation of STAT1. TNF-αphosphorylation of ERK1/ERK2 and S727 in ECV304 and smooth muscle cels. The results provide the evidences that statins may have beneficial effects by inhibiting IFN-γ action in atherosclerotic pro-cess
갑상선 세포에서 Peroxiredoxin에 의한 과산화수소 및 아포프토시스 조절
김현진,이태훈,김도희,권오유,김영건,송민호,노흥규,박수정,김호,박은신,정효균,서재미,채수홍 대한내분비학회 2000 Endocrinology and metabolism Vol.15 No.1
Background : Peroxiredoxins(Prx) play an important role in regulating cellular differentiation and proliferation in several types of mammalian cells. One mechanism for this action involves modulation of hydrogen peroxide(H2O2)-mediated cellular responses. This report examines the expression of Prx I and Prx II in thyroid cells and their roles in eliminating H2O2 produced in response to TSH. Methods : The expression of Prx-I and Prx-II were quantiated in FRTL-5 after stimulation with Thyroid stimulating hormone (TSH), Forskolin (FSK), Methimazole (MMI) and hydrogen peroxide (H2O2). Transient transfections were carried out with FRTL-5 cells at 80% confluency and 20?g of pCRprx I and pCRprx II or equivalent molar amounts of the pCR3.1TM basic vector. Transient transfection used an electroporation technique. Intracellular H2O2 was assayed in FRTL-5 cells with a fluorescent dye, 2', 7'-dichlorofluoresceindiacetate(DCFH-DA). Apoptosis of cells were evaluated by using an detection kit (Promega, Inc., Madison, WI). Results : Prx I and Prx II are constitutively expressed in FRTL-5 thyroid cells. Prx I expression, but not Prx II expression, is stimulated by exposure to TSH and H2O2. In addition, methimazole(MMI) induces a high level of Prx I mRNA and protein in these cells. Overexpression of Prx I and Prx II enhance the elimination of H2O2 produced by TSH in FRTL-5 cells. Treatment with 500?M H2O2 causes apoptosis in FRTL-5 cells as evidenced by standard assays of apoptosis(i.e., terminal deoxynucleotidyl transferase deoxyuridine triphosphate-biotin nick end-labeling(TUNEL), BAX expression and PARP cleavage. Overexpression of Prx I and Prx II reduces the amount of H2O2-induced apoptosis measured by these assays. Conclusion : These results suggest that Prx I and Prx II are involved in the removal of H2O2 in thyroid cells, and can protect these cells from undergoing apoptosis. These proteins are likely to be involved in the normal physiological response to TSH-induced production of H2O2 in thyroid cells(J Kor Soc Endocrinol15:55-69, 2000).