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Cerebrovascular gene expression in spontaneously hypertensive rats

Hypertension is a hemodynamic disorder and one of the most important and well-established risk factors for vascular diseases such as stroke. Blood vessels exposed to chronic shear stress develop structural changes and remodeling of the vascular wall through many complex mechanisms. However, the mole...

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Autores principales: Grell, Anne-Sofie, Frederiksen, Simona Denise, Edvinsson, Lars, Ansar, Saema
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5589213/
https://www.ncbi.nlm.nih.gov/pubmed/28880918
http://dx.doi.org/10.1371/journal.pone.0184233
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author Grell, Anne-Sofie
Frederiksen, Simona Denise
Edvinsson, Lars
Ansar, Saema
author_facet Grell, Anne-Sofie
Frederiksen, Simona Denise
Edvinsson, Lars
Ansar, Saema
author_sort Grell, Anne-Sofie
collection PubMed
description Hypertension is a hemodynamic disorder and one of the most important and well-established risk factors for vascular diseases such as stroke. Blood vessels exposed to chronic shear stress develop structural changes and remodeling of the vascular wall through many complex mechanisms. However, the molecular mechanisms involved are not fully understood. Hypertension-susceptible genes may provide a novel insight into potential molecular mechanisms of hypertension and secondary complications associated with hypertension. The aim of this exploratory study was to identify gene expression differences in the middle cerebral arteries between 12-week-old male spontaneously hypertensive rats and their normotensive Wistar-Kyoto rats using an Affymetrix whole-transcriptome expression profiling. Quantitative PCR and western blotting were used to verify genes of interest. 169 genes were differentially expressed in the middle cerebral arteries from hypertensive compared to normotensive rats. The gene expression of 72 genes was decreased and the gene expression of 97 genes was increased. The following genes with a fold difference ≥1.40 were verified by quantitative PCR; Postn, Olr1, Fas, Vldlr, Mmp2, Timp1, Serpine1, Mmp11, Cd34, Ptgs1 and Ptgs2. The gene expression of Postn, Olr1, Fas, Vldlr, Mmp2, Timp1 and Serpine1 and the protein expression of LOX1 (also known as OLR1) were significantly increased in the middle cerebral arteries from spontaneously hypertensive rats compared to Wistar-Kyoto rats. In conclusion, the identified genes in the middle cerebral arteries from spontaneously hypertensive rats could be possible mediators of the vascular changes and secondary complications associated with hypertension. This study supports the selection of key genes to investigate in the future research of hypertension-induced end-organ damage.
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spelling pubmed-55892132017-09-15 Cerebrovascular gene expression in spontaneously hypertensive rats Grell, Anne-Sofie Frederiksen, Simona Denise Edvinsson, Lars Ansar, Saema PLoS One Research Article Hypertension is a hemodynamic disorder and one of the most important and well-established risk factors for vascular diseases such as stroke. Blood vessels exposed to chronic shear stress develop structural changes and remodeling of the vascular wall through many complex mechanisms. However, the molecular mechanisms involved are not fully understood. Hypertension-susceptible genes may provide a novel insight into potential molecular mechanisms of hypertension and secondary complications associated with hypertension. The aim of this exploratory study was to identify gene expression differences in the middle cerebral arteries between 12-week-old male spontaneously hypertensive rats and their normotensive Wistar-Kyoto rats using an Affymetrix whole-transcriptome expression profiling. Quantitative PCR and western blotting were used to verify genes of interest. 169 genes were differentially expressed in the middle cerebral arteries from hypertensive compared to normotensive rats. The gene expression of 72 genes was decreased and the gene expression of 97 genes was increased. The following genes with a fold difference ≥1.40 were verified by quantitative PCR; Postn, Olr1, Fas, Vldlr, Mmp2, Timp1, Serpine1, Mmp11, Cd34, Ptgs1 and Ptgs2. The gene expression of Postn, Olr1, Fas, Vldlr, Mmp2, Timp1 and Serpine1 and the protein expression of LOX1 (also known as OLR1) were significantly increased in the middle cerebral arteries from spontaneously hypertensive rats compared to Wistar-Kyoto rats. In conclusion, the identified genes in the middle cerebral arteries from spontaneously hypertensive rats could be possible mediators of the vascular changes and secondary complications associated with hypertension. This study supports the selection of key genes to investigate in the future research of hypertension-induced end-organ damage. Public Library of Science 2017-09-07 /pmc/articles/PMC5589213/ /pubmed/28880918 http://dx.doi.org/10.1371/journal.pone.0184233 Text en © 2017 Grell et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Grell, Anne-Sofie
Frederiksen, Simona Denise
Edvinsson, Lars
Ansar, Saema
Cerebrovascular gene expression in spontaneously hypertensive rats
title Cerebrovascular gene expression in spontaneously hypertensive rats
title_full Cerebrovascular gene expression in spontaneously hypertensive rats
title_fullStr Cerebrovascular gene expression in spontaneously hypertensive rats
title_full_unstemmed Cerebrovascular gene expression in spontaneously hypertensive rats
title_short Cerebrovascular gene expression in spontaneously hypertensive rats
title_sort cerebrovascular gene expression in spontaneously hypertensive rats
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5589213/
https://www.ncbi.nlm.nih.gov/pubmed/28880918
http://dx.doi.org/10.1371/journal.pone.0184233
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