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CXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosis
dc.creator | Petrović-Đergović, D. | |
dc.creator | Popović, Milan | |
dc.creator | Chittiprol, S. | |
dc.creator | Cortado, H. | |
dc.creator | Ransom, R. F. | |
dc.creator | Partida-Sanchez, S. | |
dc.date.accessioned | 2018-03-01T16:04:17Z | |
dc.date.available | 2018-03-01T16:04:17Z | |
dc.date.issued | 2015 | |
dc.identifier.issn | 0009-9104 | |
dc.identifier.issn | 1365-2249 | |
dc.identifier.uri | https://vinar.vin.bg.ac.rs/handle/123456789/503 | |
dc.description.abstract | The 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.relation | info:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/175085/RS// | |
dc.relation | National 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.rights | openAccess | en |
dc.source | Clinical and Experimental Immunology | en |
dc.subject | chemokines | en |
dc.subject | CXCL10 | en |
dc.subject | kidney injury | en |
dc.subject | macrophages | en |
dc.subject | nephrotic syndrome | en |
dc.title | CXCL10 induces the recruitment of monocyte-derived macrophages into kidney, which aggravate puromycin aminonucleoside nephrosis | en |
dc.type | article | en |
dcterms.abstract | Цортадо, Х.; Цхиттипрол, С.; Петровиц-Дјерговиц, Д.; Поповиц, М.; Партида-Санцхез, С.; Рансом, Р. Ф.; | |
dc.citation.volume | 180 | |
dc.citation.issue | 2 | |
dc.citation.spage | 305 | |
dc.citation.epage | 315 | |
dc.identifier.wos | 000353048900015 | |
dc.identifier.doi | 10.1111/cei.12579 | |
dc.citation.rank | M22 | |
dc.identifier.pmid | 25561167 | |
dc.type.version | publishedVersion | |
dc.identifier.scopus | 2-s2.0-84927605689 | |
dc.identifier.fulltext | https://vinar.vin.bg.ac.rs//bitstream/id/4805/cei12579.pdf |