Genes influencing circadian differences in blood pressure in hypertensive mice.

Essential hypertension is a common multifactorial heritable condition in which increased sympathetic outflow from the central nervous system is involved in the elevation in blood pressure (BP), as well as the exaggerated morning surge in BP that is a risk factor for myocardial infarction and stroke...

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Autores principales: Francine Z Marques, Anna E Campain, Pamela J Davern, Yee Hwa J Yang, Geoffrey A Head, Brian J Morris
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Publicado: Public Library of Science (PLoS) 2011
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spelling oai:doaj.org-article:cd6521f2940048bd8203c0eba946df792021-11-18T06:55:08ZGenes influencing circadian differences in blood pressure in hypertensive mice.1932-620310.1371/journal.pone.0019203https://doaj.org/article/cd6521f2940048bd8203c0eba946df792011-04-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21541337/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Essential hypertension is a common multifactorial heritable condition in which increased sympathetic outflow from the central nervous system is involved in the elevation in blood pressure (BP), as well as the exaggerated morning surge in BP that is a risk factor for myocardial infarction and stroke in hypertensive patients. The Schlager BPH/2J mouse is a genetic model of hypertension in which increased sympathetic outflow from the hypothalamus has an important etiological role in the elevation of BP. Schlager hypertensive mice exhibit a large variation in BP between the active and inactive periods of the day, and also show a morning surge in BP. To investigate the genes responsible for the circadian variation in BP in hypertension, hypothalamic tissue was collected from BPH/2J and normotensive BPN/3J mice at the 'peak' (n = 12) and 'trough' (n = 6) of diurnal BP. Using Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays, validation by quantitative real-time PCR and a statistical method that adjusted for clock genes, we identified 212 hypothalamic genes whose expression differed between 'peak' and 'trough' BP in the hypertensive strain. These included genes with known roles in BP regulation, such as vasopressin, oxytocin and thyrotropin releasing hormone, as well as genes not recognized previously as regulators of BP, including chemokine (C-C motif) ligand 19, hypocretin and zinc finger and BTB domain containing 16. Gene ontology analysis showed an enrichment of terms for inflammatory response, mitochondrial proton-transporting ATP synthase complex, structural constituent of ribosome, amongst others. In conclusion, we have identified genes whose expression differs between the peak and trough of 24-hour circadian BP in BPH/2J mice, pointing to mechanisms responsible for diurnal variation in BP. The findings may assist in the elucidation of the mechanism for the morning surge in BP in essential hypertension.Francine Z MarquesAnna E CampainPamela J DavernYee Hwa J YangGeoffrey A HeadBrian J MorrisPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 4, p e19203 (2011)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Francine Z Marques
Anna E Campain
Pamela J Davern
Yee Hwa J Yang
Geoffrey A Head
Brian J Morris
Genes influencing circadian differences in blood pressure in hypertensive mice.
description Essential hypertension is a common multifactorial heritable condition in which increased sympathetic outflow from the central nervous system is involved in the elevation in blood pressure (BP), as well as the exaggerated morning surge in BP that is a risk factor for myocardial infarction and stroke in hypertensive patients. The Schlager BPH/2J mouse is a genetic model of hypertension in which increased sympathetic outflow from the hypothalamus has an important etiological role in the elevation of BP. Schlager hypertensive mice exhibit a large variation in BP between the active and inactive periods of the day, and also show a morning surge in BP. To investigate the genes responsible for the circadian variation in BP in hypertension, hypothalamic tissue was collected from BPH/2J and normotensive BPN/3J mice at the 'peak' (n = 12) and 'trough' (n = 6) of diurnal BP. Using Affymetrix GeneChip® Mouse Gene 1.0 ST Arrays, validation by quantitative real-time PCR and a statistical method that adjusted for clock genes, we identified 212 hypothalamic genes whose expression differed between 'peak' and 'trough' BP in the hypertensive strain. These included genes with known roles in BP regulation, such as vasopressin, oxytocin and thyrotropin releasing hormone, as well as genes not recognized previously as regulators of BP, including chemokine (C-C motif) ligand 19, hypocretin and zinc finger and BTB domain containing 16. Gene ontology analysis showed an enrichment of terms for inflammatory response, mitochondrial proton-transporting ATP synthase complex, structural constituent of ribosome, amongst others. In conclusion, we have identified genes whose expression differs between the peak and trough of 24-hour circadian BP in BPH/2J mice, pointing to mechanisms responsible for diurnal variation in BP. The findings may assist in the elucidation of the mechanism for the morning surge in BP in essential hypertension.
format article
author Francine Z Marques
Anna E Campain
Pamela J Davern
Yee Hwa J Yang
Geoffrey A Head
Brian J Morris
author_facet Francine Z Marques
Anna E Campain
Pamela J Davern
Yee Hwa J Yang
Geoffrey A Head
Brian J Morris
author_sort Francine Z Marques
title Genes influencing circadian differences in blood pressure in hypertensive mice.
title_short Genes influencing circadian differences in blood pressure in hypertensive mice.
title_full Genes influencing circadian differences in blood pressure in hypertensive mice.
title_fullStr Genes influencing circadian differences in blood pressure in hypertensive mice.
title_full_unstemmed Genes influencing circadian differences in blood pressure in hypertensive mice.
title_sort genes influencing circadian differences in blood pressure in hypertensive mice.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/cd6521f2940048bd8203c0eba946df79
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