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dc.creatorPetrovic-Djergovic, D.
dc.creatorPopović, Milan
dc.creatorChittiprol, S.
dc.creatorCortado, H.
dc.creatorRansom, R. F.
dc.creatorPartida-Sanchez, S.
dc.date.accessioned2018-03-01T16:04:17Z
dc.date.available2018-03-01T16:04:17Z
dc.date.issued2015
dc.identifier.issn0009-9104 (print)
dc.identifier.issn1365-2249 (electronic)
dc.identifier.urihttp://vinar.vin.bg.ac.rs/handle/123456789/503
dc.description.abstractThe mechanism responsible for trafficking of monocyte-derived macrophages into kidney in the puromycin aminonucleoside model of nephrotic syndrome in rats (PAN-NS), and the significance of this infiltration, remain largely unknown. CXCL10, a chemokine secreted in many T helper type 1 (Th1) inflammatory diseases, exhibits important roles in trafficking of monocytes and activated T cells. We hypothesized that induction of circulating interferon (IFN)- and glomerular tumour necrosis factor (TNF)- during PAN-NS would stimulate the release of CXCL10 by podocytes, leading to infiltration of activated immune cells and greater glomerular injury. We found that serum IFN-, glomerular Cxcl10mRNA and intra- and peri-glomerular macrophage infiltration were induced strongly during the late acute phase of PAN-NS in Wistar rats, but not in nude (Foxn1(rnu/rnu)) rats lacking functional effector T lymphocytes. Wistar rats also developed significantly greater proteinuria than nude rats, which could be abolished by macrophage depletion. Stimulation of cultured podocytes with both IFN- and TNF- markedly induced the expression of Cxcl10mRNA and CXCL10 secretion. Together, these data support our hypothesis that increased circulating IFN- and glomerular TNF- induce synergistically the production and secretion of CXCL10 by podocytes, attracting activated macrophages into kidney tissue. The study also suggests that IFN-, secreted from Th1 lymphocytes, may prime proinflammatory macrophages that consequently aggravate renal injury.en
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175085/RS//
dc.relationNational Institutes of Health: National Institute for Diabetes, Digestive and Kidney Disorders [R01-DK07553], National Institutes of Health: National Institute of Allergy and Infectious Diseases [R01-AI092117]
dc.rightsopenAccessen
dc.sourceClinical and Experimental Immunologyen
dc.subjectchemokinesen
dc.subjectCXCL10en
dc.subjectkidney injuryen
dc.subjectmacrophagesen
dc.subjectnephrotic syndromeen
dc.titleCXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosisen
dc.typearticleen
dcterms.abstractЦортадо, Х.; Цхиттипрол, С.; Петровиц-Дјерговиц, Д.; Поповиц, М.; Партида-Санцхез, С.; Рансом, Р. Ф.;
dc.citation.volume180
dc.citation.issue2
dc.citation.spage305
dc.citation.epage315
dc.identifier.wos000353048900015
dc.identifier.doi10.1111/cei.12579
dc.citation.rankM22
dc.identifier.pmid25561167
dc.identifier.scopus2-s2.0-84927605689
dc.identifier.fulltexthttp://vinar.vin.bg.ac.rs//bitstream/id/4805/cei12579.pdf


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