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Upregulation of Heme Oxygenase-1 as a Host Mechanism for Protection Against Nitric Oxide–induced Damage in Human Renal Epithelial Cells
University of Kalmar, School of Pure and Applied Natural Sciences. (Marine Microbial Ecology)
University of Kalmar, School of Pure and Applied Natural Sciences.
University of Kalmar, School of Pure and Applied Natural Sciences.
2009 (English)In: Urology, ISSN 0090-4295, E-ISSN 1527-9995, Vol. 73, no 5, 749-753 p.Article in journal (Refereed) Published
Abstract [en]

ObjectivesTo examine whether urinary tract infection–associated stimuli could regulate heme oxygenase-1 (HO-1) expression and to asses the significance of HO-1 in protecting urinary tract epithelial cells against nitric oxide (NO)-induced damage.

MethodsHeme oxygenase-1 expression was investigated in the human renal epithelial cell line A498 in response to the uropathogenic Escherichia coli (UPEC) strain IA2, the NO-donor DETA/NONOate (DETA/NO), and proinflammatory cytokines (interleukin-1β, tumor necrosis factor-α, and interferon-γ) using reverse transcriptase polymerase chain reaction and Western blot analysis. Cell viability was examined by the trypan blue exclusion test and light microscopy.

ResultsThe HO-1 inducer hemin and DETA/NO increased HO-1 expression in A498 cells, and glutathione depletion further increased HO-1 expression in response to DETA/NO and hemin. Stimulation with a UPEC strain or cytokines did not upregulate HO-1 expression. The cytokines induced inducible NO synthase expression and caused an increase in nitrite production. Hemin significantly decreased cytokine-induced NO production (P <0.001). DETA/NO decreased the cell viability by approximately 75%, but hemin was able to attenuate DETA/NO-induced cell damage.

ConclusionsThe expression of HO-1 increased in human renal epithelial cells in response to NO, and the expression was further enhanced in glutathione-depleted cells. The bacteria per se or proinflammatory cytokines were not able to upregulate HO-1. Heme oxygenase-1 protects the cells against NO by feedback inhibition of NO production and by decreasing cell damage.

Place, publisher, year, edition, pages
2009. Vol. 73, no 5, 749-753 p.
National Category
Microbiology in the medical area
Research subject
Natural Science, Biomedical Sciences
Identifiers
URN: urn:nbn:se:lnu:diva-29099DOI: 10.1016/j.urology.2008.02.027OAI: oai:DiVA.org:lnu-29099DiVA: diva2:652309
Available from: 2013-09-30 Created: 2013-09-30 Last updated: 2017-12-06Bibliographically approved
In thesis
1. Nitric oxide and bacteria-host interactions in Escherichia coli urinary tract infection
Open this publication in new window or tab >>Nitric oxide and bacteria-host interactions in Escherichia coli urinary tract infection
2008 (English)Doctoral thesis, comprehensive summary (Other academic)
Place, publisher, year, edition, pages
Kalmar: Högskolan i Kalmar, 2008. 53 p.
Series
Dissertation series / University of Kalmar, Faculty of Natural Science, ISSN 1650-2779 ; 51
National Category
Microbiology in the medical area
Research subject
Biomedical Sciences, Pharmacology
Identifiers
urn:nbn:se:lnu:diva-29096 (URN)978-91-85993-01-7 (ISBN)
Public defence
2008-04-25, Västergårds hörsal, Smålandsgatan 26b, Kalmar, 10:00
Opponent
Supervisors
Available from: 2013-11-20 Created: 2013-09-30 Last updated: 2017-01-24Bibliographically approved

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Svensson, LovisaMohlin, CamillaPersson, Katarina

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