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dc.contributor.author
Smedlund, Kathryn B.
dc.contributor.author
Birnbaumer, Lutz
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dc.contributor.author
Vazquez, Guillermo
dc.date.available
2020-04-08T17:37:19Z
dc.date.issued
2015-04
dc.identifier.citation
Smedlund, Kathryn B.; Birnbaumer, Lutz; Vazquez, Guillermo; Increased size and cellularity of advanced atherosclerotic lesions in mice with endothelial overexpression of the human TRPC3 channel; National Academy of Sciences; Proceedings of the National Academy of Sciences of The United States of America; 112; 17; 4-2015; E2201-E2206
dc.identifier.issn
0027-8424
dc.identifier.uri
http://hdl.handle.net/11336/102259
dc.description.abstract
In previous in vitro studies, we showed that Transient Receptor Potential Canonical 3 (TRPC3), a calcium-permeable, nonselective cation channel endowed with high constitutive function, is an obligatory component of the inflammatory signaling that controls expression of the vascular cell adhesion molecule-1 (VCAM-1) and monocyte adhesion to coronary artery endothelial cells. Also, TRPC3 expression in these cells was found to be up-regulated by proatherogenic factors, which enhanced inflammation and VCAM-1 expression. However, it remained to be determined whether these in vitro findings were of relevance to atherosclerotic lesion development in vivo. To answer this important question in the present work, we generated mice with endothelial-specific overexpression of human TRPC3 in an Apoe knockout background (TgEST3ApoeKO) and examined lesions in the aortic sinus following 10 and 16 wk on a high-fat diet. No significant differences were found in size or complexity of early stage lesions (10 wk). However, advanced plaques (16 wk) from TgEST3ApoeKO mice exhibited a significant increase in size and macrophage content compared with nontransgenic littermate controls. Remarkably, this change was correlated with increased VCAM-1 and phospho-IkBα immunoreactivity along the endothelial lining of lesions from transgenic animals compared with controls. These findings validate the in vivo relevance of previous in vitro findings and represent, to our knowledge, the first in vivo evidence for a proatherogenic role of endothelial TRPC3.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
National Academy of Sciences
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
aterosclerosis
dc.subject
TRPC3
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Increased size and cellularity of advanced atherosclerotic lesions in mice with endothelial overexpression of the human TRPC3 channel
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-03-16T14:06:30Z
dc.journal.volume
112
dc.journal.number
17
dc.journal.pagination
E2201-E2206
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Washington DC
dc.description.fil
Fil: Smedlund, Kathryn B.. University of Toledo College of Medicine; Estados Unidos
dc.description.fil
Fil: Birnbaumer, Lutz. National Institute of Environmental Health Sciences; Estados Unidos. Comisión Nacional de Investigación Científica y Tecnológica; Chile
dc.description.fil
Fil: Vazquez, Guillermo. University of Toledo College of Medicine; Estados Unidos
dc.journal.title
Proceedings of the National Academy of Sciences of The United States of America
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.ncbi.nlm.nih.gov/pubmed/25870279
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1073/pnas.1505410112
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.pnas.org/content/112/17/E2201
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