دورية أكاديمية
Protein-bound uremic toxins stimulate crosstalk between leukocytes and vessel wall
| العنوان: | Protein-bound uremic toxins stimulate crosstalk between leukocytes and vessel wall |
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| المؤلفون: | Pletinck, Anneleen, Glorieux, Griet, Schepers, Eva, Cohen, Gerald, Gondouin, Bertrand, Van Landschoot, Maria, Eloot, Sunny, Rops, Angelique, Van de Voorde, Johan, De Vriese, An, van der Vlag, Johan, Brunet, Philippe, Van Biesen, Wim, Vanholder, Raymond |
| المصدر: | JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY ; ISSN: 1046-6673 |
| سنة النشر: | 2013 |
| المجموعة: | Ghent University Academic Bibliography |
| مصطلحات موضوعية: | Medicine and Health Sciences, FREE P-CRESOL, CHRONIC-RENAL-FAILURE, INDOXYL SULFATE, HEMODIALYSIS-PATIENTS, HEPARAN-SULFATE, CARDIOVASCULAR-DISEASE, OXIDATIVE STRESS, IN-VIVO, GLOMERULAR ENDOTHELIAL-CELLS, CHRONIC KIDNEY-DISEASE |
| الوصف: | Leukocyte activation and endothelial damage both contribute to cardiovascular disease, a major cause of morbidity and mortality in CKD. Experimental in vitro data link several protein-bound uremic retention solutes to the modulation of inflammatory stimuli, including endothelium and leukocyte responses and cardiovascular damage, corroborating observational in vivo data. However, the impact of these uremic toxins on the crosstalk between endothelium and leukocytes has not been assessed. This study evaluated the effects of acute and continuous exposure to uremic levels of indoxylsulfate (IS), p-cresylsulfate (pCS), and p-cresylglucuronide (pCG) on the recruitment of circulating leukocytes in the rat peritoneal vascular bed using intravital microscopy. Superfusion with IS induced strong leukocyte adhesion, enhanced extravasation, and interrupted blood flow, whereas pCS caused a rapid increase in leukocyte rolling. Superfusion with pCS and pCG combined caused impaired blood flow and vascular leakage but did not further enhance leukocyte rolling over pCS alone. Intravenous infusion with IS confirmed the superfusion results and caused shedding of heparan sulfate, pointing to disruption of the glycocalyx as the mechanism likely mediating IS-induced flow stagnation. These results provide the first clear in vivo evidence that IS, pCS, and pCG exert proinflammatory effects that contribute to vascular damage by stimulating crosstalk between leukocytes and vessels. |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | application/pdf |
| اللغة: | English |
| العلاقة: | https://biblio.ugent.be/publication/4267941Test; http://hdl.handle.net/1854/LU-4267941Test; http://dx.doi.org/10.1681/ASN.2012030281Test; https://biblio.ugent.be/publication/4267941/file/4298443Test |
| DOI: | 10.1681/ASN.2012030281 |
| الإتاحة: | https://doi.org/10.1681/ASN.2012030281Test https://biblio.ugent.be/publication/4267941Test http://hdl.handle.net/1854/LU-4267941Test https://biblio.ugent.be/publication/4267941/file/4298443Test |
| حقوق: | No license (in copyright) ; info:eu-repo/semantics/restrictedAccess |
| رقم الانضمام: | edsbas.E7CCD63C |
| قاعدة البيانات: | BASE |
| DOI: | 10.1681/ASN.2012030281 |
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