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DC Field | Value | Language |
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dc.contributor.author | Kretschmar, Catalina | - |
dc.contributor.author | Oyarzún, Carlos | - |
dc.contributor.author | Villablanca, Cristopher | - |
dc.contributor.author | Jaramillo, Catherinne | - |
dc.contributor.author | Alarcón, Sebastián | - |
dc.contributor.author | Perez, Gustavo | - |
dc.contributor.author | Díaz-Encarnación, Montserrat M. M. | - |
dc.contributor.author | Pastor Anglada, Marçal | - |
dc.contributor.author | Garrido, Wallys | - |
dc.contributor.author | Quezada, Claudia | - |
dc.contributor.author | San Martín, Rody | - |
dc.date.accessioned | 2016-12-07T13:11:58Z | - |
dc.date.available | 2016-12-07T13:11:58Z | - |
dc.date.issued | 2016-01-25 | - |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://hdl.handle.net/2445/104525 | - |
dc.description.abstract | Altered nucleoside levels may be linked to pathogenic signaling through adenosine recep- tors. We hypothesized that adenosine dysregulation contributes to fibrosis in diabetic kid- ney disease. Our findings indicate that high glucose levels and experimental diabetes decreased uptake activity through the equilibrative nucleoside transporter 1 (ENT1) in proxi- mal tubule cells. In addition, a correlation between increased plasma content of adenosine and a marker of renal fibrosis in diabetic rats was evidenced. At the cellular level, exposure of HK2 cells to high glucose, TGF- β and the general adenosine receptor agonist NECA, induced the expression of profibrotic cell activation markers α -SMA and fibronectin. These effects can be avoided by using a selective antagonist of the adenosine A 3 receptor subtype in vitro. Furthermore, induction of fibrosis marker α -SMA was prevented by the A 3 receptor antagonist in diabetic rat kidneys. In conclusion, we evidenced the contribution of purinergic signaling to renal fibrosis in experimental diabetic nephropathy. | - |
dc.format.extent | 20 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Public Library of Science (PLoS) | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.1371/journal.pone.0147430 | - |
dc.relation.ispartof | PLoS One, 2016, vol. 11, num. 1, p. e0147430 | - |
dc.relation.uri | https://doi.org/10.1371/journal.pone.0147430 | - |
dc.rights | cc-by (c) Kretschmar, Catalina et al., 2016 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es | - |
dc.source | Articles publicats en revistes (Bioquímica i Biomedicina Molecular) | - |
dc.subject.classification | Diabetis | - |
dc.subject.classification | Cèl·lules epitelials | - |
dc.subject.classification | Adenosina | - |
dc.subject.other | Diabetes | - |
dc.subject.other | Epithelial cells | - |
dc.subject.other | Adenosine | - |
dc.title | Reduced adenosine uptake and its contribution to signaling that mediates profibrotic activation in renal tubular epithelial cells: implication in diabetic nephropathy. | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 663309 | - |
dc.date.updated | 2016-12-07T13:12:03Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 26808537 | - |
Appears in Collections: | Articles publicats en revistes (Bioquímica i Biomedicina Molecular) |
Files in This Item:
File | Description | Size | Format | |
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663309.pdf | 11.04 MB | Adobe PDF | View/Open |
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