Hinkelbein, Jochen, Boehm, Lennert, Spelten, Oliver, Sander, David, Soltesz, Stefan and Braunecker, Stefan ORCID: 0000-0003-3095-764X (2015). Hyperoxia-Induced Protein Alterations in Renal Rat Tissue: A Quantitative Proteomic Approach to Identify Hyperoxia-Induced Effects in Cellular Signaling Pathways. Dis. Markers, 2015. S. 1 - 13. LONDON: HINDAWI LTD. ISSN 1875-8630

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Abstract

Introduction. In renal tissue as well as in other organs, supranormal oxygen pressure may lead to deleterious consequences on a cellular level. Additionally, hyperoxia-induced effect in cells and related free radicals may potentially contribute to renal failure. The aim of this study was to analyze time-dependent alterations of rat kidney protein expression after short-term normobaric hyperoxia using proteomics and bioinformatic approaches. Material and Methods. N = 36 Wistar rats were randomized into six different groups: three groups with normobaric hyperoxia (exposure to 100% oxygen for 3 h) and three groups with normobaric normoxia (NN; room air). After hyperoxia exposure, kidneys were removed immediately, after 3 days and after 7 days. Kidney lysates were analyzed by two-dimensional gel electrophoresis followed by peptide mass fingerprinting using tandem mass spectrometry. Statistical analysis was performed with DeCyder 2D software (p < 0.01). Biological functions of differential regulated proteins were studied using functional network analysis (Ingenuity Pathways Analysis and PathwayStudio). Results. Expression of 14 proteins was significantly altered (p < 0.01): eight proteins (MEP1A_RAT, RSSA_RAT, F16P1_RAT, STML2_RAT, BPNT1_RAT, LGMN_RAT, ATPA_RAT, and VDAC1_RAT) were downregulated and six proteins (MTUS1_RAT, F16P1_RAT, ACTG_RAT, ACTB_RAT, 2ABA_RAT, and RAB1A_RAT) were upregulated. Bioinformatic analyses revealed an association of regulated proteins with inflammation. Conclusions. Significant alterations in renal protein expression could be demonstrated for up to 7 days even after short-term hyperoxia. The identified proteins indicate an association with inflammation signaling cascades. MEP1A and VDAC1 could be promising candidates to identify hyperoxic injury in kidney cells.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Hinkelbein, JochenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Boehm, LennertUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Spelten, OliverUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Sander, DavidUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Soltesz, StefanUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Braunecker, StefanUNSPECIFIEDorcid.org/0000-0003-3095-764XUNSPECIFIED
URN: urn:nbn:de:hbz:38-416411
DOI: 10.1155/2015/964263
Journal or Publication Title: Dis. Markers
Volume: 2015
Page Range: S. 1 - 13
Date: 2015
Publisher: HINDAWI LTD
Place of Publication: LONDON
ISSN: 1875-8630
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
SUPEROXIDE-DISMUTASE; LUNG INJURY; MEPRIN-A; OXYGEN; EXPRESSION; DEATH; APOPTOSIS; KIDNEY; METALLOPROTEINASE; METABOLOMEMultiple languages
Biotechnology & Applied Microbiology; Genetics & Heredity; Medicine, Research & Experimental; PathologyMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/41641

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