Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.

Patients with systemic lupus erythematosus (SLE) have a high risk of developing cardiovascular disease; however, the mechanisms involved in the early onset of atherosclerosis in these patients are not clear. Scavenger receptors, CD36 and CD163 are expressed by mononuclear phagocytes and participate...

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Autores:
Montoya Peláez, Guillermo León
Tipo de recurso:
Article of investigation
Fecha de publicación:
2011
Institución:
Universidad ICESI
Repositorio:
Repositorio ICESI
Idioma:
eng
OAI Identifier:
oai:repository.icesi.edu.co:10906/79859
Acceso en línea:
http://www.ncbi.nlm.nih.gov/pubmed/21231894
http://hdl.handle.net/10906/79859
https://doi.org/10.3109/08916934.2010.530626
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openAccess
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https://creativecommons.org/licenses/by-nc-nd/4.0/
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network_name_str Repositorio ICESI
repository_id_str
spelling Montoya Peláez, Guillermo León2016-08-30T22:01:49Z2016-08-30T22:01:49Z2011-06-140896-8411http://www.ncbi.nlm.nih.gov/pubmed/21231894http://hdl.handle.net/10906/79859https://doi.org/10.3109/08916934.2010.530626instname: Universidad Icesireponame: Biblioteca Digitalrepourl: https://repository.icesi.edu.co/Patients with systemic lupus erythematosus (SLE) have a high risk of developing cardiovascular disease; however, the mechanisms involved in the early onset of atherosclerosis in these patients are not clear. Scavenger receptors, CD36 and CD163 are expressed by mononuclear phagocytes and participate in the binding and uptake of oxidized low-density lipoproteins (Ox-LDL), contributing to foam-cells formation and atherosclerosis development. The aim of the present study was to evaluate CD36(+) and CD163(+) expression and Ox-LDL removal by monocytes from SLE and atherosclerotic patients, compared to similar age-range healthy controls. Healthy controls, SLE, and atherosclerotic patients were evaluated for carotid intima media thickness (CIMT), lipid profile, and native LDL (N-LDL) and Ox-LDL binding/endocytosis. SLE patients presented decreased high-density lipoproteins (HDL) and increased Triglyceride levels, and half of the SLE patients had increased CIMT, compared to their healthy controls (HC(SLE)). The number of CD14(+)CD163(+) cells was increased in atherosclerosis healthy controls (HC(Atheros)) compared to HC(SLE), but there were no differences between SLE or atherosclerotic patients and their respective healthy controls. Clearance assays revealed a similar capacity to bind/endocytose Ox-LDL by monocytes from SLE patients and HC(SLE), and an increased binding and endocytosis of Ox-LDL by monocytes from atherosclerotic patients, compared to HC(Atheros). The decreased CD36 and CD163 expression observed in atherosclerotic and SLE patients, respectively, suggest that these inflammatory conditions modulate these receptors differentially. The increased CIMT observed in SLE patients cannot be explained by Ox-LDL binding/endocytosis, which was comparable to their controls.engJournal of Autoimmunity, Vol. 44, No. 3 - 2011EL AUTOR, expresa que la obra objeto de la presente autorización es original y la elaboró sin quebrantar ni suplantar los derechos de autor de terceros, y de tal forma, la obra es de su exclusiva autoría y tiene la titularidad sobre éste. PARÁGRAFO: en caso de queja o acción por parte de un tercero referente a los derechos de autor sobre el artículo, folleto o libro en cuestión, EL AUTOR, asumirá la responsabilidad total, y saldrá en defensa de los derechos aquí autorizados; para todos los efectos, la Universidad Icesi actúa como un tercero de buena fe. Esta autorización, permite a la Universidad Icesi, de forma indefinida, para que en los términos establecidos en la Ley 23 de 1982, la Ley 44 de 1993, leyes y jurisprudencia vigente al respecto, haga publicación de este con fines educativos. Toda persona que consulte ya sea la biblioteca o en medio electrónico podrá copiar apartes del texto citando siempre la fuentes, es decir el título del trabajo y el autor.https://creativecommons.org/licenses/by-nc-nd/4.0/info:eu-repo/semantics/openAccessAtribución-NoComercial-SinDerivadas 4.0 Internacional (CC BY-NC-ND 4.0)http://purl.org/coar/access_right/c_abf2Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.info:eu-repo/semantics/articlehttp://purl.org/coar/resource_type/c_2df8fbb1Artículoinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/version/c_970fb48d4fbd8a8544ORIGINALdocumento.htmldocumento.htmltext/html300http://repository.icesi.edu.co/biblioteca_digital/bitstream/10906/79859/1/documento.htmlb26fa7724f175c173093a11b83112f06MD5110906/79859oai:repository.icesi.edu.co:10906/798592020-05-26 23:40:44.638Biblioteca Digital - Universidad icesicdcriollo@icesi.edu.co
dc.title.eng.fl_str_mv Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
title Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
spellingShingle Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
title_short Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
title_full Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
title_fullStr Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
title_full_unstemmed Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
title_sort Atherosclerosis development in SLE patients is not determined by monocytes ability to bind/endocytose Ox-LDL.
dc.creator.fl_str_mv Montoya Peláez, Guillermo León
dc.contributor.author.spa.fl_str_mv Montoya Peláez, Guillermo León
description Patients with systemic lupus erythematosus (SLE) have a high risk of developing cardiovascular disease; however, the mechanisms involved in the early onset of atherosclerosis in these patients are not clear. Scavenger receptors, CD36 and CD163 are expressed by mononuclear phagocytes and participate in the binding and uptake of oxidized low-density lipoproteins (Ox-LDL), contributing to foam-cells formation and atherosclerosis development. The aim of the present study was to evaluate CD36(+) and CD163(+) expression and Ox-LDL removal by monocytes from SLE and atherosclerotic patients, compared to similar age-range healthy controls. Healthy controls, SLE, and atherosclerotic patients were evaluated for carotid intima media thickness (CIMT), lipid profile, and native LDL (N-LDL) and Ox-LDL binding/endocytosis. SLE patients presented decreased high-density lipoproteins (HDL) and increased Triglyceride levels, and half of the SLE patients had increased CIMT, compared to their healthy controls (HC(SLE)). The number of CD14(+)CD163(+) cells was increased in atherosclerosis healthy controls (HC(Atheros)) compared to HC(SLE), but there were no differences between SLE or atherosclerotic patients and their respective healthy controls. Clearance assays revealed a similar capacity to bind/endocytose Ox-LDL by monocytes from SLE patients and HC(SLE), and an increased binding and endocytosis of Ox-LDL by monocytes from atherosclerotic patients, compared to HC(Atheros). The decreased CD36 and CD163 expression observed in atherosclerotic and SLE patients, respectively, suggest that these inflammatory conditions modulate these receptors differentially. The increased CIMT observed in SLE patients cannot be explained by Ox-LDL binding/endocytosis, which was comparable to their controls.
publishDate 2011
dc.date.issued.none.fl_str_mv 2011-06-14
dc.date.accessioned.none.fl_str_mv 2016-08-30T22:01:49Z
dc.date.available.none.fl_str_mv 2016-08-30T22:01:49Z
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dc.identifier.doi.none.fl_str_mv https://doi.org/10.3109/08916934.2010.530626
dc.identifier.instname.none.fl_str_mv instname: Universidad Icesi
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identifier_str_mv 0896-8411
instname: Universidad Icesi
reponame: Biblioteca Digital
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url http://www.ncbi.nlm.nih.gov/pubmed/21231894
http://hdl.handle.net/10906/79859
https://doi.org/10.3109/08916934.2010.530626
dc.language.iso.eng.fl_str_mv eng
language eng
dc.relation.ispartof.eng.fl_str_mv Journal of Autoimmunity, Vol. 44, No. 3 - 2011
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dc.rights.accessrights.eng.fl_str_mv info:eu-repo/semantics/openAccess
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eu_rights_str_mv openAccess
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