Evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia

Macrophages are a heterogeneous population with both pro- and anti-inflammatory functions play an essential role in maintaining tissue homeostasis, promoting inflammation under pathological conditions, and tissue repair after injury. In pulmonary hypertension, the M1 phenotype is more pro-inflammato...

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Autores principales:	Vijaya Karoor, Delaney Swindle, David I Pak, Derek Strassheim, Mehdi A Fini, Edward Dempsey, Kurt R Stenmark, Kathryn Hassell, Rachelle Nuss, Paul W. Buehler, David C. Irwin
Formato:	article
Lenguaje:	EN
Publicado:	SAGE Publishing 2021
Materias:	Diseases of the circulatory (Cardiovascular) system RC666-701 Diseases of the respiratory system RC705-779
Acceso en línea:	https://doaj.org/article/120e16e92c14421486d903082b393f81
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spelling	oai:doaj.org-article:120e16e92c14421486d903082b393f812021-11-05T22:04:15ZEvidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia2045-894010.1177/20458940211056806https://doaj.org/article/120e16e92c14421486d903082b393f812021-11-01T00:00:00Zhttps://doi.org/10.1177/20458940211056806https://doaj.org/toc/2045-8940Macrophages are a heterogeneous population with both pro- and anti-inflammatory functions play an essential role in maintaining tissue homeostasis, promoting inflammation under pathological conditions, and tissue repair after injury. In pulmonary hypertension, the M1 phenotype is more pro-inflammatory compared to the M2 phenotype, which is involved in tissue repair. The role of macrophages in the initiation and progression of pulmonary hypertension is well studied. However, their role in the regression of established pulmonary hypertension is not well known. Rats chronically exposed to hemoglobin (Hb) plus hypoxia (HX) share similarities to humans with pulmonary hypertension associated with hemolytic disease, including the presence of a unique macrophage phenotype surrounding distal vessels that are associated with vascular remodeling. These lung macrophages are characterized by high iron content, HO-1, ET-1, and IL-6, and are recruited from the circulation. Depletion of macrophages in this model prevents the development of pulmonary hypertension and vascular remodeling. In this study, we specifically investigate the regression of pulmonary hypertension over a four-week duration after rats were removed from Hb + HX exposure with and without gadolinium chloride administration. Withdrawal of Hb + HX reversed systolic pressures and right ventricular function after Hb + Hx exposure in four weeks. Our data show that depleting circulating monocytes/macrophages during reversal prevents complete recovery of right ventricular systolic pressure and vascular remodeling in this rat model of pulmonary hypertension at four weeks post exposure. The data presented offer a novel insight into the role of macrophages in the processes of pulmonary hypertension regression in a rodent model of Hb + Hx-driven disease.Vijaya KaroorDelaney SwindleDavid I PakDerek StrassheimMehdi A FiniEdward DempseyKurt R StenmarkKathryn HassellRachelle NussPaul W. BuehlerDavid C. IrwinSAGE PublishingarticleDiseases of the circulatory (Cardiovascular) systemRC666-701Diseases of the respiratory systemRC705-779ENPulmonary Circulation, Vol 11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Diseases of the circulatory (Cardiovascular) system RC666-701 Diseases of the respiratory system RC705-779
spellingShingle	Diseases of the circulatory (Cardiovascular) system RC666-701 Diseases of the respiratory system RC705-779 Vijaya Karoor Delaney Swindle David I Pak Derek Strassheim Mehdi A Fini Edward Dempsey Kurt R Stenmark Kathryn Hassell Rachelle Nuss Paul W. Buehler David C. Irwin Evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia
description	Macrophages are a heterogeneous population with both pro- and anti-inflammatory functions play an essential role in maintaining tissue homeostasis, promoting inflammation under pathological conditions, and tissue repair after injury. In pulmonary hypertension, the M1 phenotype is more pro-inflammatory compared to the M2 phenotype, which is involved in tissue repair. The role of macrophages in the initiation and progression of pulmonary hypertension is well studied. However, their role in the regression of established pulmonary hypertension is not well known. Rats chronically exposed to hemoglobin (Hb) plus hypoxia (HX) share similarities to humans with pulmonary hypertension associated with hemolytic disease, including the presence of a unique macrophage phenotype surrounding distal vessels that are associated with vascular remodeling. These lung macrophages are characterized by high iron content, HO-1, ET-1, and IL-6, and are recruited from the circulation. Depletion of macrophages in this model prevents the development of pulmonary hypertension and vascular remodeling. In this study, we specifically investigate the regression of pulmonary hypertension over a four-week duration after rats were removed from Hb + HX exposure with and without gadolinium chloride administration. Withdrawal of Hb + HX reversed systolic pressures and right ventricular function after Hb + Hx exposure in four weeks. Our data show that depleting circulating monocytes/macrophages during reversal prevents complete recovery of right ventricular systolic pressure and vascular remodeling in this rat model of pulmonary hypertension at four weeks post exposure. The data presented offer a novel insight into the role of macrophages in the processes of pulmonary hypertension regression in a rodent model of Hb + Hx-driven disease.
format	article
author	Vijaya Karoor Delaney Swindle David I Pak Derek Strassheim Mehdi A Fini Edward Dempsey Kurt R Stenmark Kathryn Hassell Rachelle Nuss Paul W. Buehler David C. Irwin
author_facet	Vijaya Karoor Delaney Swindle David I Pak Derek Strassheim Mehdi A Fini Edward Dempsey Kurt R Stenmark Kathryn Hassell Rachelle Nuss Paul W. Buehler David C. Irwin
author_sort	Vijaya Karoor
title	Evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia
title_short	Evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia
title_full	Evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia
title_fullStr	Evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia
title_full_unstemmed	Evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia
title_sort	evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia
publisher	SAGE Publishing
publishDate	2021
url	https://doaj.org/article/120e16e92c14421486d903082b393f81
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Evidence supporting a role for circulating macrophages in the regression of vascular remodeling following sub-chronic exposure to hemoglobin plus hypoxia

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