Stem Cell Factor Expression after Renal Ischemia Promotes Tubular Epithelial Survival

Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the tubular basement membrane. Survival of the tubular epithelium following ischemia is therefore important in the successful regeneration of renal ti...

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Veröffentlicht in:	PloS one Jg. 5; H. 12; S. e14386
Hauptverfasser:	Stokman, Geurt, Stroo, Ingrid, Claessen, Nike, Teske, Gwendoline J. D., Weening, Jan J., Leemans, Jaklien C., Florquin, Sandrine
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Public Library of Science 21.12.2010 Public Library of Science (PLoS)
Schlagworte:	Animals Antisense oligonucleotides Apoptosis Autocrine signalling Basement Membrane - metabolism c-Kit protein Cell Biology/Cell Signaling Cell Biology/Cellular Death and Stress Responses Cell Survival Epidermal growth factor Epithelial cells Epithelial Cells - cytology Epithelium Gene Expression Regulation Hypoxia Immunology/Immune Response Ischemia Ischemia - pathology Kidney - pathology Kidney Tubules - metabolism Kidneys Kinases Ligands Male Mice Mice, Inbred C57BL Nephrology/Acute Renal Failure Oligonucleotides Phosphorylation Proto-Oncogene Proteins c-kit - metabolism Regeneration Renal function Reperfusion Rodents Stem cell factor Stem Cell Factor - biosynthesis Stem cells Survival Tubular basement membrane Netherlands
ISSN:	1932-6203, 1932-6203
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Abstract	Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the tubular basement membrane. Survival of the tubular epithelium following ischemia is therefore important in the successful regeneration of renal tissue. The cytokine stem cell factor (SCF) has been shown to protect the tubular epithelium against apoptosis. In a mouse model for renal ischemia/reperfusion injury, we studied how expression of c-KIT on tubular epithelium and its ligand SCF protect cells against apoptosis. Administration of SCF specific antisense oligonucleotides significantly decreased specific staining of SCF following ischemia. Reduced SCF expression resulted in impaired renal function, increased tubular damage and increased tubular epithelial apoptosis, independent of inflammation. In an in vitro hypoxia model, stimulation of tubular epithelial cells with SCF activated survival signaling and decreased apoptosis. Our data indicate an important role for c-KIT and SCF in mediating tubular epithelial cell survival via an autocrine pathway.
AbstractList	Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the tubular basement membrane. Survival of the tubular epithelium following ischemia is therefore important in the successful regeneration of renal tissue. The cytokine stem cell factor (SCF) has been shown to protect the tubular epithelium against apoptosis.BACKGROUNDRenal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the tubular basement membrane. Survival of the tubular epithelium following ischemia is therefore important in the successful regeneration of renal tissue. The cytokine stem cell factor (SCF) has been shown to protect the tubular epithelium against apoptosis.In a mouse model for renal ischemia/reperfusion injury, we studied how expression of c-KIT on tubular epithelium and its ligand SCF protect cells against apoptosis. Administration of SCF specific antisense oligonucleotides significantly decreased specific staining of SCF following ischemia. Reduced SCF expression resulted in impaired renal function, increased tubular damage and increased tubular epithelial apoptosis, independent of inflammation. In an in vitro hypoxia model, stimulation of tubular epithelial cells with SCF activated survival signaling and decreased apoptosis.METHODOLOGY/PRINCIPAL FINDINGSIn a mouse model for renal ischemia/reperfusion injury, we studied how expression of c-KIT on tubular epithelium and its ligand SCF protect cells against apoptosis. Administration of SCF specific antisense oligonucleotides significantly decreased specific staining of SCF following ischemia. Reduced SCF expression resulted in impaired renal function, increased tubular damage and increased tubular epithelial apoptosis, independent of inflammation. In an in vitro hypoxia model, stimulation of tubular epithelial cells with SCF activated survival signaling and decreased apoptosis.Our data indicate an important role for c-KIT and SCF in mediating tubular epithelial cell survival via an autocrine pathway.CONCLUSIONS/SIGNIFICANCEOur data indicate an important role for c-KIT and SCF in mediating tubular epithelial cell survival via an autocrine pathway. BACKGROUND: Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the tubular basement membrane. Survival of the tubular epithelium following ischemia is therefore important in the successful regeneration of renal tissue. The cytokine stem cell factor (SCF) has been shown to protect the tubular epithelium against apoptosis. METHODOLOGY/PRINCIPAL FINDINGS: In a mouse model for renal ischemia/reperfusion injury, we studied how expression of c-KIT on tubular epithelium and its ligand SCF protect cells against apoptosis. Administration of SCF specific antisense oligonucleotides significantly decreased specific staining of SCF following ischemia. Reduced SCF expression resulted in impaired renal function, increased tubular damage and increased tubular epithelial apoptosis, independent of inflammation. In an in vitro hypoxia model, stimulation of tubular epithelial cells with SCF activated survival signaling and decreased apoptosis. CONCLUSIONS/SIGNIFICANCE: Our data indicate an important role for c-KIT and SCF in mediating tubular epithelial cell survival via an autocrine pathway. Background Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the tubular basement membrane. Survival of the tubular epithelium following ischemia is therefore important in the successful regeneration of renal tissue. The cytokine stem cell factor (SCF) has been shown to protect the tubular epithelium against apoptosis. Methodology/Principal Findings In a mouse model for renal ischemia/reperfusion injury, we studied how expression of c-KIT on tubular epithelium and its ligand SCF protect cells against apoptosis. Administration of SCF specific antisense oligonucleotides significantly decreased specific staining of SCF following ischemia. Reduced SCF expression resulted in impaired renal function, increased tubular damage and increased tubular epithelial apoptosis, independent of inflammation. In an in vitro hypoxia model, stimulation of tubular epithelial cells with SCF activated survival signaling and decreased apoptosis. Conclusions/Significance Our data indicate an important role for c-KIT and SCF in mediating tubular epithelial cell survival via an autocrine pathway. Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the tubular basement membrane. Survival of the tubular epithelium following ischemia is therefore important in the successful regeneration of renal tissue. The cytokine stem cell factor (SCF) has been shown to protect the tubular epithelium against apoptosis. In a mouse model for renal ischemia/reperfusion injury, we studied how expression of c-KIT on tubular epithelium and its ligand SCF protect cells against apoptosis. Administration of SCF specific antisense oligonucleotides significantly decreased specific staining of SCF following ischemia. Reduced SCF expression resulted in impaired renal function, increased tubular damage and increased tubular epithelial apoptosis, independent of inflammation. In an in vitro hypoxia model, stimulation of tubular epithelial cells with SCF activated survival signaling and decreased apoptosis. Our data indicate an important role for c-KIT and SCF in mediating tubular epithelial cell survival via an autocrine pathway. Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the tubular basement membrane. Survival of the tubular epithelium following ischemia is therefore important in the successful regeneration of renal tissue. The cytokine stem cell factor (SCF) has been shown to protect the tubular epithelium against apoptosis. In a mouse model for renal ischemia/reperfusion injury, we studied how expression of c-KIT on tubular epithelium and its ligand SCF protect cells against apoptosis. Administration of SCF specific antisense oligonucleotides significantly decreased specific staining of SCF following ischemia. Reduced SCF expression resulted in impaired renal function, increased tubular damage and increased tubular epithelial apoptosis, independent of inflammation. In an in vitro hypoxia model, stimulation of tubular epithelial cells with SCF activated survival signaling and decreased apoptosis. Our data indicate an important role for c-KIT and SCF in mediating tubular epithelial cell survival via an autocrine pathway.
Audience	Academic
Author	Stroo, Ingrid Weening, Jan J. Stokman, Geurt Claessen, Nike Florquin, Sandrine Teske, Gwendoline J. D. Leemans, Jaklien C.
AuthorAffiliation	Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands University of Hong Kong, Hong Kong
AuthorAffiliation_xml	– name: University of Hong Kong, Hong Kong – name: Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
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BackLink	https://www.ncbi.nlm.nih.gov/pubmed/21200435$$D View this record in MEDLINE/PubMed
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceived and designed the experiments: GS JW JCL SF. Performed the experiments: GS IS NC GT. Analyzed the data: GS SF. Contributed reagents/materials/analysis tools: GS. Wrote the paper: GS IS JCL. Current address: Division of Toxicology, LACDR, Leiden University, Leiden, The Netherlands
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Snippet	Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization of the... Background Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization... BACKGROUND: Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization... Background Renal ischemia leads to apoptosis of tubular epithelial cells and results in decreased renal function. Tissue repair involves re-epithelialization...
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SubjectTerms	Animals Antisense oligonucleotides Apoptosis Autocrine signalling Basement Membrane - metabolism c-Kit protein Cell Biology/Cell Signaling Cell Biology/Cellular Death and Stress Responses Cell Survival Epidermal growth factor Epithelial cells Epithelial Cells - cytology Epithelium Gene Expression Regulation Hypoxia Immunology/Immune Response Ischemia Ischemia - pathology Kidney - pathology Kidney Tubules - metabolism Kidneys Kinases Ligands Male Mice Mice, Inbred C57BL Nephrology/Acute Renal Failure Oligonucleotides Phosphorylation Proto-Oncogene Proteins c-kit - metabolism Regeneration Renal function Reperfusion Rodents Stem cell factor Stem Cell Factor - biosynthesis Stem cells Survival Tubular basement membrane
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Title	Stem Cell Factor Expression after Renal Ischemia Promotes Tubular Epithelial Survival
URI	https://www.ncbi.nlm.nih.gov/pubmed/21200435 https://www.proquest.com/docview/1296288685 https://www.proquest.com/docview/822556365 https://pubmed.ncbi.nlm.nih.gov/PMC3006174 https://doaj.org/article/053ea80e865c4c268869e00cda6d01c7 http://dx.doi.org/10.1371/journal.pone.0014386
Volume	5
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