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Conference Paper: Chemokines usage by tubular epithelial cells in IgA nephropathy: role of TNF-α and Angiotensin II

TitleChemokines usage by tubular epithelial cells in IgA nephropathy: role of TNF-α and Angiotensin II
Authors
Issue Date2012
PublisherAmerican Society of Nephrology. The Journal's web site is located at https://www.asn-online.org/abstracts/
Citation
Kidney Week 2012, San Diego, CA., 30 October-4 November 2012. In Journal of the American Society of Nephrology, 2012, v. 23, p. 854A, abstract no. SA-PO930 How to Cite?
AbstractBACKGROUND: Tubulointerstitial infiltration of immunocompetent cells is associated with a rapid progression in IgA nephropathy (IgAN). We examined the role of tumor necrosis factor-α (TNF-α) and angiotensin II (AngII) in tubular chemokines usage in IgAN. METHODS: Using a transwell co-culture system, we studied the chemokines usage and chemotactic responses of peripheral blood mononuclear cells (PBMC) towards proximal tubular epithelial cells (PTEC) following activation by conditioned medium prepared from mesangial cells cultured with IgA from IgAN patients (IgA-medium; n=45) and healthy subjects (n=30). RESULTS: Increased expression of chemokines, including CXCL1, CXCL2, CXCL8, CCL2, CCL5 and CCL11, was observed in PTEC cultured with IgA-medium. In response to IgA-medium, chemotaxis of CD45+ PBMC, and in particular, the activated GMP- 17+, CD3+ lymphocytes and CD14+ monocytes towards PTEC were increased. The transmigrated subsets exhibited differential up-regulated expression of CXCR2, CCR2 and CCR5. Chemotactic response of activated CD3+ cells was attenuated by anti-CCL5, followed by anti-CCL2 but not by anti-CXCL1 or anti-CXCL2. Transmigrated activated CD14+ cells was reduced by anti-CCL2, anti-CCL5 and anti-CXCL2. Transmigrated activated GMP-17+ was inhibited by anti-CCL5. Under all circumstances, anti-CCL11 have no effect on the cellular transmigration. PTEC activated by IgA-medium had elevated expression of AngII, transforming growth factor-β (TGF-β) and TNF-α. The release of CXCL1, CXCL2, CXCL8, CCL2, CCL5 and CCL11, was increased by TNF-α, but not by TGF-β. AngII priming further increase all chemokines examined. Synthesis of chemokines and transmigration after activation of PTEC with IgA-medium was blocked by anti-TNF-α or losartan, but not by anti-TGF-β or PD123319 (AT2R blocker). Interestingly, TGF-β blockage enhanced the apoptosis of transmigrated GMP17+ subset. CONCLUSIONS: Our data show the differential chemotactic responses of PBMC subsets towards PTEC in IgAN. These events utilize different chemokine-chemokine receptor axes and are tightly regulated through the interaction of IgA-medium induced TNF-α and AngII.
DescriptionSaturday Poster Presentation - Probing the Immune Basis of Glomerular and Intersitial Kidney Diseases - II: no. SA-PO930
Persistent Identifierhttp://hdl.handle.net/10722/186846
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699

 

DC FieldValueLanguage
dc.contributor.authorLim, AIen_US
dc.contributor.authorTang, SCWen_US
dc.contributor.authorChan, LYYen_US
dc.contributor.authorLai, KNen_US
dc.contributor.authorLeung, JCKen_US
dc.date.accessioned2013-08-20T12:21:13Z-
dc.date.available2013-08-20T12:21:13Z-
dc.date.issued2012en_US
dc.identifier.citationKidney Week 2012, San Diego, CA., 30 October-4 November 2012. In Journal of the American Society of Nephrology, 2012, v. 23, p. 854A, abstract no. SA-PO930en_US
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/186846-
dc.descriptionSaturday Poster Presentation - Probing the Immune Basis of Glomerular and Intersitial Kidney Diseases - II: no. SA-PO930-
dc.description.abstractBACKGROUND: Tubulointerstitial infiltration of immunocompetent cells is associated with a rapid progression in IgA nephropathy (IgAN). We examined the role of tumor necrosis factor-α (TNF-α) and angiotensin II (AngII) in tubular chemokines usage in IgAN. METHODS: Using a transwell co-culture system, we studied the chemokines usage and chemotactic responses of peripheral blood mononuclear cells (PBMC) towards proximal tubular epithelial cells (PTEC) following activation by conditioned medium prepared from mesangial cells cultured with IgA from IgAN patients (IgA-medium; n=45) and healthy subjects (n=30). RESULTS: Increased expression of chemokines, including CXCL1, CXCL2, CXCL8, CCL2, CCL5 and CCL11, was observed in PTEC cultured with IgA-medium. In response to IgA-medium, chemotaxis of CD45+ PBMC, and in particular, the activated GMP- 17+, CD3+ lymphocytes and CD14+ monocytes towards PTEC were increased. The transmigrated subsets exhibited differential up-regulated expression of CXCR2, CCR2 and CCR5. Chemotactic response of activated CD3+ cells was attenuated by anti-CCL5, followed by anti-CCL2 but not by anti-CXCL1 or anti-CXCL2. Transmigrated activated CD14+ cells was reduced by anti-CCL2, anti-CCL5 and anti-CXCL2. Transmigrated activated GMP-17+ was inhibited by anti-CCL5. Under all circumstances, anti-CCL11 have no effect on the cellular transmigration. PTEC activated by IgA-medium had elevated expression of AngII, transforming growth factor-β (TGF-β) and TNF-α. The release of CXCL1, CXCL2, CXCL8, CCL2, CCL5 and CCL11, was increased by TNF-α, but not by TGF-β. AngII priming further increase all chemokines examined. Synthesis of chemokines and transmigration after activation of PTEC with IgA-medium was blocked by anti-TNF-α or losartan, but not by anti-TGF-β or PD123319 (AT2R blocker). Interestingly, TGF-β blockage enhanced the apoptosis of transmigrated GMP17+ subset. CONCLUSIONS: Our data show the differential chemotactic responses of PBMC subsets towards PTEC in IgAN. These events utilize different chemokine-chemokine receptor axes and are tightly regulated through the interaction of IgA-medium induced TNF-α and AngII.-
dc.languageengen_US
dc.publisherAmerican Society of Nephrology. The Journal's web site is located at https://www.asn-online.org/abstracts/-
dc.relation.ispartofJASN Abstract Supplementen_US
dc.titleChemokines usage by tubular epithelial cells in IgA nephropathy: role of TNF-α and Angiotensin IIen_US
dc.typeConference_Paperen_US
dc.identifier.emailTang, SCW: scwtang@hku.hken_US
dc.identifier.emailChan, LYY: yychanb@hku.hken_US
dc.identifier.emailLai, KN: knlai@hku.hken_US
dc.identifier.emailLeung, JCK: jckleung@hku.hken_US
dc.identifier.authorityTang, SCW=rp00480en_US
dc.identifier.authorityLai, KN=rp00324en_US
dc.identifier.authorityLeung, JCK=rp00448en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros220815en_US
dc.identifier.volume23en_US
dc.identifier.spage854A, abstract no. SA-PO930en_US
dc.identifier.epage854A, abstract no. SA-PO930en_US
dc.publisher.placeUnited States-

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