Hydrogen peroxide modulates expression of surface antigens by human umbilical vein endothelial cells in vitro

被引：7

作者：

Kudryavtsev I.V. ^{[1
,2
,3
]}

Garnyuk V.V. ^{[4
]}

Nadeev A.D. ^{[5
]}

Goncharov N.V. ^{[4
,6
]}

机构：

[1] Research Institute of Experimental Medicine, Russian Academy of Medical Sciences, ul. Acad. Pavlova, 12, St. Petersburg

[2] Far-Eastern Federal University, Vladivostok

[3] St. Petersburg State University, St. Petersburg

[4] Research Institute of Hygiene, Occupational Pathology and Human Ecology, Federal Medical Biological Agency, St. Petersburg

[5] Institute of Cell Biophysics, Russian Academy of Sciences, ul. Instituskaya, 3, Pushchino, Moscow Oblast

[6] Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg

来源：

Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology | 2014年 / 8卷 / 1期

关键词：

CD antigens; endothelial cells; expression; hydrogen peroxide;

D O I：

10.1134/S1990747813050103

中图分类号：

学科分类号：

摘要：

The aim of this study was to determine the immunological phenotype of human umbilical vein endothelial cells in culture and dynamics of expression of inducible CD molecules of the endothelial cell surface exposed to hydrogen peroxide (H2O2, 100-300 μM) in vitro. PMA was applied as a positive control. There was an insignificant increase (9-21%) of CD31 expression 3 h after the addition of H2O2to the culture medium, statistically significant decrease of CD309 expression upon exposure to 200 and 300 μM H2O2, whereas a day after the addition of H2O2we found a strongly pronounced dose-dependent increase of CD54 expression, as well as a moderate enhancement of the expression of all CD molecules. © 2014 Pleiades Publishing, Ltd.

引用

页码：97 / 102

页数：5

共 29 条

[1]

Baldridge C.W., Gerard R.W., The extra respiration of phagocytosis, AJP-Legacy, 103, pp. 235-236, (1932)

[2]

Thannickal V.J., Fanburg B.L., Reactive oxygen species in cell signaling, American Journal of Physiology - Lung Cellular and Molecular Physiology, 279, 6, (2000)

[3]

Janero D.R., Hreniuk D., Suppression of TCA cycle activity in the cardiac muscle cell by hydroperoxide-induced oxidant stress, Am. J. Physiol., 270, 6 PART 1, (1996)

[4]

Shappell S.B., Toman C., Anderson D.C., Taylor A.A., Entman M.L., Smith C.W., Mac-1 (CD11b/CD18) mediates adherence-dependent hydrogen peroxide production by human and canine neutrophils, Journal of Immunology, 144, 7, pp. 2702-2711, (1990)

[5]

Jones D.P., Radical-free biology of oxidative stress, Am. J. Physiol. Cell Physiol., 295, 4, (2008)

[6]

Martin-Ventura J.L., Madrigal-Matute J., Martinez-Pinna R., Ramos-Mozo P., Blanco-Colio L.M., Moreno J.A., Tarin C., Burillo E., Fernandez-Garcia C.E., Egido J., Meilhac O., Michel J.B., Erythrocytes, leukocytes and platelets as a source of oxidative stress in chronic vascular diseases: Detoxifying mechanisms and potential therapeutic options, Thromb Haemost., 108, 3, pp. 435-442, (2012)

[7]

Gardner P.R., Nguyen D.-D.H., White C.W., Aconitase is a sensitive and critical target of oxygen poisoning in cultured mammalian cells and in rat lungs, Proceedings of the National Academy of Sciences of the United States of America, 91, 25, pp. 12248-12252, (1994)

[8]

Al Ahmad A., Gassmann M., Ogunshola O.O., Involvement of oxidative stress in hypoxia-induced blood-brain barrier breakdown, Microvasc Res., 84, 2, pp. 222-225, (2012)

[9]

Mohr S., Hallak H., De Boitte A., Lapetina E.G., Brune B., Nitric oxide-induced S-glutathionylation and inactivation of glyceraldehyde-3-phosphate dehydrogenase, J. Biol. Chem., 274, 14, pp. 9427-9430, (1999)

[10]

Neumann P., Gertzberg N., Vaughan E., Weisbrot J., Woodburn R., Lambert W., Johnson A., Peroxynitrite mediates TNF-alpha-induced endothelial barrier dysfunction and nitration of actin, American Journal of Physiology - Lung Cellular and Molecular Physiology, 290, 4, (2006)

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