Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus

Abstract Autoimmune diseases such as psoriasis, rheumatoid arthritis, and systemic lupus erythematosus (SLE) have high rates of hypertension and cardiovascular disease. Systemic lupus erythematosus is a prototypic autoimmune disorder that primarily affects women of childbearing age and is associated...

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Main Authors: Daniel M. McClung, William J. Kalusche, Katie E. Jones, Michael J. Ryan, Erin B. Taylor
Format: Article
Language:English
Published: Wiley 2021-02-01
Series:Physiological Reports
Subjects:
Online Access:https://doi.org/10.14814/phy2.14734
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author Daniel M. McClung
William J. Kalusche
Katie E. Jones
Michael J. Ryan
Erin B. Taylor
author_facet Daniel M. McClung
William J. Kalusche
Katie E. Jones
Michael J. Ryan
Erin B. Taylor
author_sort Daniel M. McClung
collection DOAJ
description Abstract Autoimmune diseases such as psoriasis, rheumatoid arthritis, and systemic lupus erythematosus (SLE) have high rates of hypertension and cardiovascular disease. Systemic lupus erythematosus is a prototypic autoimmune disorder that primarily affects women of childbearing age and is associated with a loss of self‐tolerance, autoreactive B and T lymphocytes, and the production of autoantibodies, especially to nuclear components. In this study, we hypothesized that the pristane‐inducible model of SLE would develop hypertension and vascular dysfunction as the disease progressed. To test this hypothesis, female C57BL/6 mice were administered PBS or pristane. Seven months after pristane administration, mice developed various autoantibodies, including anti‐dsDNA IgG, anti‐ssDNA IgG, and anti‐nRNP IgG, as well as hypergammaglobulinemia. Several other immunological changes, including increased circulating neutrophils and increased CD4−CD8− (double negative) thymocytes were also detected. Mean arterial pressure (MAP) was elevated in pristane‐treated mice when compared to PBS‐treated mice. In addition, second‐order mesenteric arteries from pristine‐treated mice had impaired relaxation to the endothelium‐dependent vasodilator acetylcholine compared to PBS‐treated mice. These data suggest that the immune system dysfunction present in the pristane model of lupus contributes to the development of hypertension and vascular dysfunction.
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spelling doaj.art-d9f24eeca8644853a679bb6aff943dd32022-12-21T22:43:19ZengWileyPhysiological Reports2051-817X2021-02-0193n/an/a10.14814/phy2.14734Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosusDaniel M. McClung0William J. Kalusche1Katie E. Jones2Michael J. Ryan3Erin B. Taylor4Department of Physiology and Biophysics University of Mississippi Medical Center Jackson MS USADepartment of Physiology and Biophysics University of Mississippi Medical Center Jackson MS USADepartment of Physiology and Biophysics University of Mississippi Medical Center Jackson MS USADepartment of Physiology and Biophysics University of Mississippi Medical Center Jackson MS USADepartment of Physiology and Biophysics University of Mississippi Medical Center Jackson MS USAAbstract Autoimmune diseases such as psoriasis, rheumatoid arthritis, and systemic lupus erythematosus (SLE) have high rates of hypertension and cardiovascular disease. Systemic lupus erythematosus is a prototypic autoimmune disorder that primarily affects women of childbearing age and is associated with a loss of self‐tolerance, autoreactive B and T lymphocytes, and the production of autoantibodies, especially to nuclear components. In this study, we hypothesized that the pristane‐inducible model of SLE would develop hypertension and vascular dysfunction as the disease progressed. To test this hypothesis, female C57BL/6 mice were administered PBS or pristane. Seven months after pristane administration, mice developed various autoantibodies, including anti‐dsDNA IgG, anti‐ssDNA IgG, and anti‐nRNP IgG, as well as hypergammaglobulinemia. Several other immunological changes, including increased circulating neutrophils and increased CD4−CD8− (double negative) thymocytes were also detected. Mean arterial pressure (MAP) was elevated in pristane‐treated mice when compared to PBS‐treated mice. In addition, second‐order mesenteric arteries from pristine‐treated mice had impaired relaxation to the endothelium‐dependent vasodilator acetylcholine compared to PBS‐treated mice. These data suggest that the immune system dysfunction present in the pristane model of lupus contributes to the development of hypertension and vascular dysfunction.https://doi.org/10.14814/phy2.14734autoantibodiesautoimmunityendothelial dysfunctionhypertensionpristanesystemic lupus erythematosus
spellingShingle Daniel M. McClung
William J. Kalusche
Katie E. Jones
Michael J. Ryan
Erin B. Taylor
Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus
Physiological Reports
autoantibodies
autoimmunity
endothelial dysfunction
hypertension
pristane
systemic lupus erythematosus
title Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus
title_full Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus
title_fullStr Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus
title_full_unstemmed Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus
title_short Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus
title_sort hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus
topic autoantibodies
autoimmunity
endothelial dysfunction
hypertension
pristane
systemic lupus erythematosus
url https://doi.org/10.14814/phy2.14734
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AT katieejones hypertensionandendothelialdysfunctioninthepristanemodelofsystemiclupuserythematosus
AT michaeljryan hypertensionandendothelialdysfunctioninthepristanemodelofsystemiclupuserythematosus
AT erinbtaylor hypertensionandendothelialdysfunctioninthepristanemodelofsystemiclupuserythematosus