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2015 ; 2015
(ä): 964263
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Hyperoxia-Induced Protein Alterations in Renal Rat Tissue: A Quantitative
Proteomic Approach to Identify Hyperoxia-Induced Effects in Cellular Signaling
Pathways
#MMPMID26106253
Hinkelbein J
; Böhm L
; Spelten O
; Sander D
; Soltész S
; Braunecker S
Dis Markers
2015[]; 2015
(ä): 964263
PMID26106253
show ga
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.