P-Cresol sulfate and indoxyl sulfate induce similar cellular inflammatory gene expressions in cultured proximal renal tubular cells

Chiao Yin Sun, Hsiang Hao Hsu, Mai-Szu Wu

研究成果: 雜誌貢獻文章

71 引文 (Scopus)

摘要

Backgroundp-Cresol sulfate (PCS) and indoxyl sulfate (IS) have important roles in the kidney injury. The aim of this study was to determine the inflammatory response to PCS and IS.MethodsCultured mouse proximal renal tubular cells were treated with PCS or IS and analyzed by polymerase chain reaction array with an inflammation and immune panel. Gene annotation enrichment and functional annotation clustering were analyzed with the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Functional networks of the target genes were analyzed with the algorithm GeneMANIA. Results PCS and IS increased the expression of inflammation associated genes. Sixteen upregulated gene clusters of cells treated with PCS or IS were found. The major cytokines in the functional networks generated by PCS or IS treatment were Tgfb1, Fasl, Il6/15, Il15, Csf1/3 and Cxcl10. The major intracellular signal triggered by PCS or IS included Stats, Smads, Nfkb2, Ikbkb, Bcl2 and Bax. In both PCS-and IS-treated cells, Col4a5, Cxc10, Fasl, Stat1 and Ikbkb were the target genes in the predicted molecular functional networks connected to Tgfb1.ConclusionsPCS and IS stimulate significant cellular inflammation. Similar immune and cellular inflammatory responses were induced by PCS or IS on cultured proximal renal tubular cells.

原文英語
頁(從 - 到)70-78
頁數9
期刊Nephrology Dialysis Transplantation
28
發行號1
DOIs
出版狀態已發佈 - 一月 2013
對外發佈Yes

指紋

cresol
Indican
Sulfates
Kidney
Gene Expression
Inflammation
Molecular Sequence Annotation
Interleukin-15

ASJC Scopus subject areas

  • Nephrology
  • Transplantation

引用此文

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title = "P-Cresol sulfate and indoxyl sulfate induce similar cellular inflammatory gene expressions in cultured proximal renal tubular cells",
abstract = "Backgroundp-Cresol sulfate (PCS) and indoxyl sulfate (IS) have important roles in the kidney injury. The aim of this study was to determine the inflammatory response to PCS and IS.MethodsCultured mouse proximal renal tubular cells were treated with PCS or IS and analyzed by polymerase chain reaction array with an inflammation and immune panel. Gene annotation enrichment and functional annotation clustering were analyzed with the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Functional networks of the target genes were analyzed with the algorithm GeneMANIA. Results PCS and IS increased the expression of inflammation associated genes. Sixteen upregulated gene clusters of cells treated with PCS or IS were found. The major cytokines in the functional networks generated by PCS or IS treatment were Tgfb1, Fasl, Il6/15, Il15, Csf1/3 and Cxcl10. The major intracellular signal triggered by PCS or IS included Stats, Smads, Nfkb2, Ikbkb, Bcl2 and Bax. In both PCS-and IS-treated cells, Col4a5, Cxc10, Fasl, Stat1 and Ikbkb were the target genes in the predicted molecular functional networks connected to Tgfb1.ConclusionsPCS and IS stimulate significant cellular inflammation. Similar immune and cellular inflammatory responses were induced by PCS or IS on cultured proximal renal tubular cells.",
keywords = "gene ontology, indoxyl sulfate, inflammation, p-cresol sulfate",
author = "Sun, {Chiao Yin} and Hsu, {Hsiang Hao} and Mai-Szu Wu",
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AU - Hsu, Hsiang Hao

AU - Wu, Mai-Szu

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Y1 - 2013/1

N2 - Backgroundp-Cresol sulfate (PCS) and indoxyl sulfate (IS) have important roles in the kidney injury. The aim of this study was to determine the inflammatory response to PCS and IS.MethodsCultured mouse proximal renal tubular cells were treated with PCS or IS and analyzed by polymerase chain reaction array with an inflammation and immune panel. Gene annotation enrichment and functional annotation clustering were analyzed with the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Functional networks of the target genes were analyzed with the algorithm GeneMANIA. Results PCS and IS increased the expression of inflammation associated genes. Sixteen upregulated gene clusters of cells treated with PCS or IS were found. The major cytokines in the functional networks generated by PCS or IS treatment were Tgfb1, Fasl, Il6/15, Il15, Csf1/3 and Cxcl10. The major intracellular signal triggered by PCS or IS included Stats, Smads, Nfkb2, Ikbkb, Bcl2 and Bax. In both PCS-and IS-treated cells, Col4a5, Cxc10, Fasl, Stat1 and Ikbkb were the target genes in the predicted molecular functional networks connected to Tgfb1.ConclusionsPCS and IS stimulate significant cellular inflammation. Similar immune and cellular inflammatory responses were induced by PCS or IS on cultured proximal renal tubular cells.

AB - Backgroundp-Cresol sulfate (PCS) and indoxyl sulfate (IS) have important roles in the kidney injury. The aim of this study was to determine the inflammatory response to PCS and IS.MethodsCultured mouse proximal renal tubular cells were treated with PCS or IS and analyzed by polymerase chain reaction array with an inflammation and immune panel. Gene annotation enrichment and functional annotation clustering were analyzed with the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Functional networks of the target genes were analyzed with the algorithm GeneMANIA. Results PCS and IS increased the expression of inflammation associated genes. Sixteen upregulated gene clusters of cells treated with PCS or IS were found. The major cytokines in the functional networks generated by PCS or IS treatment were Tgfb1, Fasl, Il6/15, Il15, Csf1/3 and Cxcl10. The major intracellular signal triggered by PCS or IS included Stats, Smads, Nfkb2, Ikbkb, Bcl2 and Bax. In both PCS-and IS-treated cells, Col4a5, Cxc10, Fasl, Stat1 and Ikbkb were the target genes in the predicted molecular functional networks connected to Tgfb1.ConclusionsPCS and IS stimulate significant cellular inflammation. Similar immune and cellular inflammatory responses were induced by PCS or IS on cultured proximal renal tubular cells.

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