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Metabolomic analysis of Shiga toxin 2a-induced injury in conditionally immortalized glomerular endothelial cells
C. Patry, K. Plotnicki, C. Betzen, AP. Ortiz, KL. Pappan, SC. Satchell, PW. Mathieson, M. Bielaszewska, H. Karch, B. Tönshoff, N. Rafat,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
ProQuest Central
od 2005-03-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 2005-03-01 do Před 1 rokem
- MeSH
- endoteliální buňky cytologie účinky léků metabolismus MeSH
- glomerulus cytologie MeSH
- kultivované buňky MeSH
- lidé MeSH
- lipopolysacharidy MeSH
- metabolomika * MeSH
- multivariační analýza MeSH
- počet buněk MeSH
- shiga toxin 2 metabolismus farmakologie MeSH
- viabilita buněk účinky léků MeSH
- zánět chemicky indukované metabolismus patologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
INTRODUCTION: Shiga toxin 2a (Stx2a) induces hemolytic uremic syndrome (STEC HUS) by targeting glomerular endothelial cells (GEC). OBJECTIVES: We investigated in a metabolomic analysis the response of a conditionally immortalized, stable glomerular endothelial cell line (ciGEnC) to Stx2a stimulation as a cell culture model for STEC HUS. METHODS: CiGEnC were treated with tumor necrosis factor-(TNF)α, Stx2a or sequentially with TNFα and Stx2a. We performed a metabolomic high-throughput screening by lipid- or gas chromatography and subsequent mass spectrometry. Metabolite fold changes in stimulated ciGEnC compared to untreated cells were calculated. RESULTS: 320 metabolites were identified and investigated. In response to TNFα + Stx2a, there was a predominant increase in intracellular free fatty acids and amino acids. Furthermore, lipid- and protein derived pro-inflammatory mediators, oxidative stress and an augmented intracellular energy turnover were increased in ciGEnC. Levels of most biochemicals related to carbohydrate metabolism remained unchanged. CONCLUSION: Stimulation of ciGEnC with TNFα + Stx2a is associated with profound metabolic changes indicative of increased inflammation, oxidative stress and energy turnover.
Department of Pediatrics 1 University Children's Hospital Heidelberg 69120 Heidelberg Germany
Institute for Hygiene University of Münster 48149 Münster Germany
Learning and Research Southmead Hospital Bristol University of Bristol Bristol BS8 1TH UK
Metabolon Inc 617 Davis Drive Suite 400 Durham NC 27713 USA
The Principal's Office University of Edinburgh Edinburgh EH8 9YL UK
Citace poskytuje Crossref.org
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- $a Patry, Christian $u Department of Pediatrics I, University Children's Hospital Heidelberg, 69120, Heidelberg, Germany. Division of Cardiovascular Physiology, Institute of Physiology and Pathophysiology, University of Heidelberg, 69120, Heidelberg, Germany.
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- $a Metabolomic analysis of Shiga toxin 2a-induced injury in conditionally immortalized glomerular endothelial cells / $c C. Patry, K. Plotnicki, C. Betzen, AP. Ortiz, KL. Pappan, SC. Satchell, PW. Mathieson, M. Bielaszewska, H. Karch, B. Tönshoff, N. Rafat,
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- $a INTRODUCTION: Shiga toxin 2a (Stx2a) induces hemolytic uremic syndrome (STEC HUS) by targeting glomerular endothelial cells (GEC). OBJECTIVES: We investigated in a metabolomic analysis the response of a conditionally immortalized, stable glomerular endothelial cell line (ciGEnC) to Stx2a stimulation as a cell culture model for STEC HUS. METHODS: CiGEnC were treated with tumor necrosis factor-(TNF)α, Stx2a or sequentially with TNFα and Stx2a. We performed a metabolomic high-throughput screening by lipid- or gas chromatography and subsequent mass spectrometry. Metabolite fold changes in stimulated ciGEnC compared to untreated cells were calculated. RESULTS: 320 metabolites were identified and investigated. In response to TNFα + Stx2a, there was a predominant increase in intracellular free fatty acids and amino acids. Furthermore, lipid- and protein derived pro-inflammatory mediators, oxidative stress and an augmented intracellular energy turnover were increased in ciGEnC. Levels of most biochemicals related to carbohydrate metabolism remained unchanged. CONCLUSION: Stimulation of ciGEnC with TNFα + Stx2a is associated with profound metabolic changes indicative of increased inflammation, oxidative stress and energy turnover.
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- $a Plotnicki, Kathrin $u Department of Pediatrics I, University Children's Hospital Heidelberg, 69120, Heidelberg, Germany.
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- $a Bielaszewska, Martina $u Institute for Hygiene, University of Münster, 48149, Münster, Germany. Reference Laboratory for E. coli and Shigella, National Public Health Institute, Srobarova 48, 10042, Prague, Czech Republic.
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- $a Rafat, Neysan $u Department of Pediatrics I, University Children's Hospital Heidelberg, 69120, Heidelberg, Germany. Neysan.Rafat@umm.de. Department of Neonatology, University Children's Hospital Mannheim, University of Heidelberg, 68167, Mannheim, Germany. Neysan.Rafat@umm.de. Department of Pharmaceutical Sciences, Bahá'í Institute of Higher Education (BIHE), Teheran, Iran. Neysan.Rafat@umm.de.
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