TWEAK (tumor necrosis factor–like weak inducer of apoptosis) activates CXCL16 expression during renal tubulointerstitial inflammation
TWEAK (tumor necrosis factor–like weak inducer of apoptosis) is a TNF superfamily cytokine that activates the fibroblast growth factor–inducible 14 (Fn14) receptor. Transcriptional analysis of experimental kidney tubulointerstitial inflammation showed a correlation between an upregulation of the mRN...
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| Veröffentlicht in: | Kidney international 2012-06, Vol.81 (11), p.1098-1107 |
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| creator | Izquierdo, María Concepción Sanz, Ana B. Mezzano, Sergio Blanco, Julia Carrasco, Susana Sanchez-Niño, María Dolores Benito-Martín, Alberto Ruiz-Ortega, Marta Egido, Jesús Ortiz, Alberto |
| description | TWEAK (tumor necrosis factor–like weak inducer of apoptosis) is a TNF superfamily cytokine that activates the fibroblast growth factor–inducible 14 (Fn14) receptor. Transcriptional analysis of experimental kidney tubulointerstitial inflammation showed a correlation between an upregulation of the mRNA for the transmembrane chemokine CXCL16, a T-cell chemoattractant, and Fn14 activation. Exogenous TWEAK increased mouse kidney CXCL16 expression and T-lymphocyte infiltration in vivo, processes inhibited by the NF-κB inhibitor parthenolide. Tubular cell CXCL16 was increased in a nephrotoxic tubulointerstitial inflammation model and neutralizing anti-TWEAK antibodies decreased this CXCL16 expression and lymphocyte infiltration. In human kidney biopsies with tubulointerstitial inflammation, tubular cell CXCL16 and Fn14 expressions were associated with inflammatory infiltrates. TWEAK upregulated CXCL16 mRNA expression in cultured renal tubular cells in an NF-κB-dependent manner and increased soluble and cellular CXCL16 protein. CXCL16 modestly promoted the expression of cytokines in tubular cells expressing its receptor (CXCR6) and appeared to synergize with TWEAK to promote an inflammatory response; however, it did not modulate tubular cell proliferation or survival. Thus, TWEAK upregulates the expression of the chemokine CXCL16 in tubular epithelium and this may contribute to kidney tubulointerstitial inflammation. |
| doi_str_mv | 10.1038/ki.2011.475 |
| format | Article |
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Transcriptional analysis of experimental kidney tubulointerstitial inflammation showed a correlation between an upregulation of the mRNA for the transmembrane chemokine CXCL16, a T-cell chemoattractant, and Fn14 activation. Exogenous TWEAK increased mouse kidney CXCL16 expression and T-lymphocyte infiltration in vivo, processes inhibited by the NF-κB inhibitor parthenolide. Tubular cell CXCL16 was increased in a nephrotoxic tubulointerstitial inflammation model and neutralizing anti-TWEAK antibodies decreased this CXCL16 expression and lymphocyte infiltration. In human kidney biopsies with tubulointerstitial inflammation, tubular cell CXCL16 and Fn14 expressions were associated with inflammatory infiltrates. TWEAK upregulated CXCL16 mRNA expression in cultured renal tubular cells in an NF-κB-dependent manner and increased soluble and cellular CXCL16 protein. CXCL16 modestly promoted the expression of cytokines in tubular cells expressing its receptor (CXCR6) and appeared to synergize with TWEAK to promote an inflammatory response; however, it did not modulate tubular cell proliferation or survival. Thus, TWEAK upregulates the expression of the chemokine CXCL16 in tubular epithelium and this may contribute to kidney tubulointerstitial inflammation.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.2011.475</identifier><identifier>PMID: 22278019</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>Basingstoke: Elsevier Inc</publisher><subject>acute kidney injury ; Adult ; Animals ; Antibodies, Neutralizing - pharmacology ; Biological and medical sciences ; Biopsy ; Cell Line ; chemokine ; Chemokine CXCL16 ; Chemokine CXCL6 - genetics ; Chemokine CXCL6 - metabolism ; Chemokines, CXC - metabolism ; Chemotaxis ; Cytokine TWEAK ; Disease Models, Animal ; Female ; Folic Acid ; Gene Expression Profiling ; Glomerulonephritis ; Humans ; inflammation ; Kidney Tubules - drug effects ; Kidney Tubules - immunology ; Kidney Tubules - metabolism ; Kidney Tubules - pathology ; Kidneys ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Middle Aged ; Nephritis, Interstitial - chemically induced ; Nephritis, Interstitial - genetics ; Nephritis, Interstitial - immunology ; Nephritis, Interstitial - metabolism ; Nephritis, Interstitial - pathology ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; NF-kappa B - antagonists & inhibitors ; NF-kappa B - metabolism ; Receptors, Scavenger - metabolism ; Receptors, Tumor Necrosis Factor - metabolism ; Recombinant Proteins - metabolism ; RNA, Messenger - metabolism ; Sesquiterpenes - pharmacology ; T-Lymphocytes - immunology ; T-Lymphocytes - metabolism ; Tumor Necrosis Factors - antagonists & inhibitors ; Tumor Necrosis Factors - immunology ; Tumor Necrosis Factors - metabolism ; TWEAK Receptor ; Up-Regulation ; Urinary system involvement in other diseases. Miscellaneous</subject><ispartof>Kidney international, 2012-06, Vol.81 (11), p.1098-1107</ispartof><rights>2012 International Society of Nephrology</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jun 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-847bfeeb82365559d49eddd683f49b2554b286026475518ad3b66bbe6ebf7c8c3</citedby><cites>FETCH-LOGICAL-c496t-847bfeeb82365559d49eddd683f49b2554b286026475518ad3b66bbe6ebf7c8c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=25907320$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22278019$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Izquierdo, María Concepción</creatorcontrib><creatorcontrib>Sanz, Ana B.</creatorcontrib><creatorcontrib>Mezzano, Sergio</creatorcontrib><creatorcontrib>Blanco, Julia</creatorcontrib><creatorcontrib>Carrasco, Susana</creatorcontrib><creatorcontrib>Sanchez-Niño, María Dolores</creatorcontrib><creatorcontrib>Benito-Martín, Alberto</creatorcontrib><creatorcontrib>Ruiz-Ortega, Marta</creatorcontrib><creatorcontrib>Egido, Jesús</creatorcontrib><creatorcontrib>Ortiz, Alberto</creatorcontrib><title>TWEAK (tumor necrosis factor–like weak inducer of apoptosis) activates CXCL16 expression during renal tubulointerstitial inflammation</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>TWEAK (tumor necrosis factor–like weak inducer of apoptosis) is a TNF superfamily cytokine that activates the fibroblast growth factor–inducible 14 (Fn14) receptor. Transcriptional analysis of experimental kidney tubulointerstitial inflammation showed a correlation between an upregulation of the mRNA for the transmembrane chemokine CXCL16, a T-cell chemoattractant, and Fn14 activation. Exogenous TWEAK increased mouse kidney CXCL16 expression and T-lymphocyte infiltration in vivo, processes inhibited by the NF-κB inhibitor parthenolide. Tubular cell CXCL16 was increased in a nephrotoxic tubulointerstitial inflammation model and neutralizing anti-TWEAK antibodies decreased this CXCL16 expression and lymphocyte infiltration. In human kidney biopsies with tubulointerstitial inflammation, tubular cell CXCL16 and Fn14 expressions were associated with inflammatory infiltrates. TWEAK upregulated CXCL16 mRNA expression in cultured renal tubular cells in an NF-κB-dependent manner and increased soluble and cellular CXCL16 protein. CXCL16 modestly promoted the expression of cytokines in tubular cells expressing its receptor (CXCR6) and appeared to synergize with TWEAK to promote an inflammatory response; however, it did not modulate tubular cell proliferation or survival. Thus, TWEAK upregulates the expression of the chemokine CXCL16 in tubular epithelium and this may contribute to kidney tubulointerstitial inflammation.</description><subject>acute kidney injury</subject><subject>Adult</subject><subject>Animals</subject><subject>Antibodies, Neutralizing - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Cell Line</subject><subject>chemokine</subject><subject>Chemokine CXCL16</subject><subject>Chemokine CXCL6 - genetics</subject><subject>Chemokine CXCL6 - metabolism</subject><subject>Chemokines, CXC - metabolism</subject><subject>Chemotaxis</subject><subject>Cytokine TWEAK</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Folic Acid</subject><subject>Gene Expression Profiling</subject><subject>Glomerulonephritis</subject><subject>Humans</subject><subject>inflammation</subject><subject>Kidney Tubules - drug effects</subject><subject>Kidney Tubules - immunology</subject><subject>Kidney Tubules - metabolism</subject><subject>Kidney Tubules - pathology</subject><subject>Kidneys</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Middle Aged</subject><subject>Nephritis, Interstitial - chemically induced</subject><subject>Nephritis, Interstitial - genetics</subject><subject>Nephritis, Interstitial - immunology</subject><subject>Nephritis, Interstitial - metabolism</subject><subject>Nephritis, Interstitial - pathology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>NF-kappa B - antagonists & inhibitors</subject><subject>NF-kappa B - metabolism</subject><subject>Receptors, Scavenger - metabolism</subject><subject>Receptors, Tumor Necrosis Factor - metabolism</subject><subject>Recombinant Proteins - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>Sesquiterpenes - pharmacology</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - metabolism</subject><subject>Tumor Necrosis Factors - antagonists & inhibitors</subject><subject>Tumor Necrosis Factors - immunology</subject><subject>Tumor Necrosis Factors - metabolism</subject><subject>TWEAK Receptor</subject><subject>Up-Regulation</subject><subject>Urinary system involvement in other diseases. 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Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>NF-kappa B - antagonists & inhibitors</topic><topic>NF-kappa B - metabolism</topic><topic>Receptors, Scavenger - metabolism</topic><topic>Receptors, Tumor Necrosis Factor - metabolism</topic><topic>Recombinant Proteins - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>Sesquiterpenes - pharmacology</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - metabolism</topic><topic>Tumor Necrosis Factors - antagonists & inhibitors</topic><topic>Tumor Necrosis Factors - immunology</topic><topic>Tumor Necrosis Factors - metabolism</topic><topic>TWEAK Receptor</topic><topic>Up-Regulation</topic><topic>Urinary system involvement in other diseases. 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Transcriptional analysis of experimental kidney tubulointerstitial inflammation showed a correlation between an upregulation of the mRNA for the transmembrane chemokine CXCL16, a T-cell chemoattractant, and Fn14 activation. Exogenous TWEAK increased mouse kidney CXCL16 expression and T-lymphocyte infiltration in vivo, processes inhibited by the NF-κB inhibitor parthenolide. Tubular cell CXCL16 was increased in a nephrotoxic tubulointerstitial inflammation model and neutralizing anti-TWEAK antibodies decreased this CXCL16 expression and lymphocyte infiltration. In human kidney biopsies with tubulointerstitial inflammation, tubular cell CXCL16 and Fn14 expressions were associated with inflammatory infiltrates. TWEAK upregulated CXCL16 mRNA expression in cultured renal tubular cells in an NF-κB-dependent manner and increased soluble and cellular CXCL16 protein. CXCL16 modestly promoted the expression of cytokines in tubular cells expressing its receptor (CXCR6) and appeared to synergize with TWEAK to promote an inflammatory response; however, it did not modulate tubular cell proliferation or survival. Thus, TWEAK upregulates the expression of the chemokine CXCL16 in tubular epithelium and this may contribute to kidney tubulointerstitial inflammation.</abstract><cop>Basingstoke</cop><pub>Elsevier Inc</pub><pmid>22278019</pmid><doi>10.1038/ki.2011.475</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Kidney international, 2012-06, Vol.81 (11), p.1098-1107 |
| issn | 0085-2538 1523-1755 |
| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | acute kidney injury Adult Animals Antibodies, Neutralizing - pharmacology Biological and medical sciences Biopsy Cell Line chemokine Chemokine CXCL16 Chemokine CXCL6 - genetics Chemokine CXCL6 - metabolism Chemokines, CXC - metabolism Chemotaxis Cytokine TWEAK Disease Models, Animal Female Folic Acid Gene Expression Profiling Glomerulonephritis Humans inflammation Kidney Tubules - drug effects Kidney Tubules - immunology Kidney Tubules - metabolism Kidney Tubules - pathology Kidneys Male Medical sciences Mice Mice, Inbred C57BL Middle Aged Nephritis, Interstitial - chemically induced Nephritis, Interstitial - genetics Nephritis, Interstitial - immunology Nephritis, Interstitial - metabolism Nephritis, Interstitial - pathology Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure NF-kappa B - antagonists & inhibitors NF-kappa B - metabolism Receptors, Scavenger - metabolism Receptors, Tumor Necrosis Factor - metabolism Recombinant Proteins - metabolism RNA, Messenger - metabolism Sesquiterpenes - pharmacology T-Lymphocytes - immunology T-Lymphocytes - metabolism Tumor Necrosis Factors - antagonists & inhibitors Tumor Necrosis Factors - immunology Tumor Necrosis Factors - metabolism TWEAK Receptor Up-Regulation Urinary system involvement in other diseases. Miscellaneous |
| title | TWEAK (tumor necrosis factor–like weak inducer of apoptosis) activates CXCL16 expression during renal tubulointerstitial inflammation |
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