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Carbon Monoxide Suppresses Neointima Formation in Transplant Arteriosclerosis by Inhibiting Vascular Progenitor Cell Differentiation

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Carbon Monoxide Suppresses Neointima Formation in Transplant Arteriosclerosis by Inhibiting Vascular Progenitor Cell Differentiation. / Sakihama, Hideyasu; Lee, Ghee Rye; Chin, Beek Y; Csizmadia, Eva; Gallo, David; Qi, Yilin; Gagliani, Nicola; Wang, Hongjun; Bach, Fritz H; Otterbein, Leo E.

in: ARTERIOSCL THROM VAS, Jahrgang 41, Nr. 6, 06.2021, S. 1915-1927.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Sakihama, H, Lee, GR, Chin, BY, Csizmadia, E, Gallo, D, Qi, Y, Gagliani, N, Wang, H, Bach, FH & Otterbein, LE 2021, 'Carbon Monoxide Suppresses Neointima Formation in Transplant Arteriosclerosis by Inhibiting Vascular Progenitor Cell Differentiation', ARTERIOSCL THROM VAS, Jg. 41, Nr. 6, S. 1915-1927. https://doi.org/10.1161/ATVBAHA.120.315558

APA

Sakihama, H., Lee, G. R., Chin, B. Y., Csizmadia, E., Gallo, D., Qi, Y., Gagliani, N., Wang, H., Bach, F. H., & Otterbein, L. E. (2021). Carbon Monoxide Suppresses Neointima Formation in Transplant Arteriosclerosis by Inhibiting Vascular Progenitor Cell Differentiation. ARTERIOSCL THROM VAS, 41(6), 1915-1927. https://doi.org/10.1161/ATVBAHA.120.315558

Vancouver

Sakihama H, Lee GR, Chin BY, Csizmadia E, Gallo D, Qi Y et al. Carbon Monoxide Suppresses Neointima Formation in Transplant Arteriosclerosis by Inhibiting Vascular Progenitor Cell Differentiation. ARTERIOSCL THROM VAS. 2021 Jun;41(6):1915-1927. https://doi.org/10.1161/ATVBAHA.120.315558

Bibtex

@article{b9963b6d55b44713bc1f89e55bd6fe04,
title = "Carbon Monoxide Suppresses Neointima Formation in Transplant Arteriosclerosis by Inhibiting Vascular Progenitor Cell Differentiation",
abstract = "Objective:Evidence indicates that bone marrow progenitor cells (BMPC) are a major contributor to neointima formation in transplant arteriosclerosis. HO-1 (heme oxygenase-1, Hmox1) and carbon monoxide (CO), a product of heme degradation by HO-1, ameliorate neointima formation by inhibiting proliferation of smooth muscle cells. We investigated the mechanism whereby HO-1 and CO modulate BMPC and mitigates neointima formation in transplant arteriosclerosis.Approach and Results:Using a murine model of aortic transplantation, bone marrow chimeric mice, and in vitro experiments, we report that CO does not inhibit mobilization of BMPC into the circulation or their homing to the vessel adventitia, but instead suppresses differentiation of BMPC into smooth muscle cells after they arrive in the adventitia. Specifically, the effect of CO on differentiation of BMPC into smooth muscle cell is mediated in part, by limiting PDGFR-β (platelet derived growth factor receptor-β) signaling. Hmox1−/− BMPC exhibit a greater propensity to differentiate into smooth muscle cell in vitro, in part by regulating PDGFR-β+ expression. Furthermore, wild-type mice transplanted with Hmox1−/− bone marrow cells show augmented neointima formation after allografting versus control. CO exposure significantly ameliorated neointima formation, which remains more severe with Hmox1−/− bone marrow cell versus air-treated mice receiving HO-1-expressing bone marrow cell, highlighting the importance of endogenous HO-1 in neointima formation.Conclusions:Host BMPC contribute to neointima formation in transplant arteriosclerosis and the protective effect afforded by HO-1/CO against neointima formation is mediated in part through the regulation of PDGFR-β expression. We propose that suppressing differentiation of BMPC is a major mechanism by which HO-1 and CO prevent neointima expansion after transplant.",
keywords = "Animals, Aorta, Thoracic/enzymology, Arteriosclerosis/enzymology, Bone Marrow Transplantation, Carbon Monoxide/pharmacology, Cell Differentiation/drug effects, Cells, Cultured, Disease Models, Animal, Heme Oxygenase-1/genetics, Kinetics, Male, Membrane Proteins/genetics, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Knockout, Muscle, Smooth, Vascular/drug effects, Myocytes, Smooth Muscle/drug effects, Neointima, Receptor, Platelet-Derived Growth Factor beta/metabolism, Stem Cells/drug effects, Transplantation Chimera, Vascular Remodeling/drug effects",
author = "Hideyasu Sakihama and Lee, {Ghee Rye} and Chin, {Beek Y} and Eva Csizmadia and David Gallo and Yilin Qi and Nicola Gagliani and Hongjun Wang and Bach, {Fritz H} and Otterbein, {Leo E}",
year = "2021",
month = jun,
doi = "10.1161/ATVBAHA.120.315558",
language = "English",
volume = "41",
pages = "1915--1927",
journal = "ARTERIOSCL THROM VAS",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

RIS

TY - JOUR

T1 - Carbon Monoxide Suppresses Neointima Formation in Transplant Arteriosclerosis by Inhibiting Vascular Progenitor Cell Differentiation

AU - Sakihama, Hideyasu

AU - Lee, Ghee Rye

AU - Chin, Beek Y

AU - Csizmadia, Eva

AU - Gallo, David

AU - Qi, Yilin

AU - Gagliani, Nicola

AU - Wang, Hongjun

AU - Bach, Fritz H

AU - Otterbein, Leo E

PY - 2021/6

Y1 - 2021/6

N2 - Objective:Evidence indicates that bone marrow progenitor cells (BMPC) are a major contributor to neointima formation in transplant arteriosclerosis. HO-1 (heme oxygenase-1, Hmox1) and carbon monoxide (CO), a product of heme degradation by HO-1, ameliorate neointima formation by inhibiting proliferation of smooth muscle cells. We investigated the mechanism whereby HO-1 and CO modulate BMPC and mitigates neointima formation in transplant arteriosclerosis.Approach and Results:Using a murine model of aortic transplantation, bone marrow chimeric mice, and in vitro experiments, we report that CO does not inhibit mobilization of BMPC into the circulation or their homing to the vessel adventitia, but instead suppresses differentiation of BMPC into smooth muscle cells after they arrive in the adventitia. Specifically, the effect of CO on differentiation of BMPC into smooth muscle cell is mediated in part, by limiting PDGFR-β (platelet derived growth factor receptor-β) signaling. Hmox1−/− BMPC exhibit a greater propensity to differentiate into smooth muscle cell in vitro, in part by regulating PDGFR-β+ expression. Furthermore, wild-type mice transplanted with Hmox1−/− bone marrow cells show augmented neointima formation after allografting versus control. CO exposure significantly ameliorated neointima formation, which remains more severe with Hmox1−/− bone marrow cell versus air-treated mice receiving HO-1-expressing bone marrow cell, highlighting the importance of endogenous HO-1 in neointima formation.Conclusions:Host BMPC contribute to neointima formation in transplant arteriosclerosis and the protective effect afforded by HO-1/CO against neointima formation is mediated in part through the regulation of PDGFR-β expression. We propose that suppressing differentiation of BMPC is a major mechanism by which HO-1 and CO prevent neointima expansion after transplant.

AB - Objective:Evidence indicates that bone marrow progenitor cells (BMPC) are a major contributor to neointima formation in transplant arteriosclerosis. HO-1 (heme oxygenase-1, Hmox1) and carbon monoxide (CO), a product of heme degradation by HO-1, ameliorate neointima formation by inhibiting proliferation of smooth muscle cells. We investigated the mechanism whereby HO-1 and CO modulate BMPC and mitigates neointima formation in transplant arteriosclerosis.Approach and Results:Using a murine model of aortic transplantation, bone marrow chimeric mice, and in vitro experiments, we report that CO does not inhibit mobilization of BMPC into the circulation or their homing to the vessel adventitia, but instead suppresses differentiation of BMPC into smooth muscle cells after they arrive in the adventitia. Specifically, the effect of CO on differentiation of BMPC into smooth muscle cell is mediated in part, by limiting PDGFR-β (platelet derived growth factor receptor-β) signaling. Hmox1−/− BMPC exhibit a greater propensity to differentiate into smooth muscle cell in vitro, in part by regulating PDGFR-β+ expression. Furthermore, wild-type mice transplanted with Hmox1−/− bone marrow cells show augmented neointima formation after allografting versus control. CO exposure significantly ameliorated neointima formation, which remains more severe with Hmox1−/− bone marrow cell versus air-treated mice receiving HO-1-expressing bone marrow cell, highlighting the importance of endogenous HO-1 in neointima formation.Conclusions:Host BMPC contribute to neointima formation in transplant arteriosclerosis and the protective effect afforded by HO-1/CO against neointima formation is mediated in part through the regulation of PDGFR-β expression. We propose that suppressing differentiation of BMPC is a major mechanism by which HO-1 and CO prevent neointima expansion after transplant.

KW - Animals

KW - Aorta, Thoracic/enzymology

KW - Arteriosclerosis/enzymology

KW - Bone Marrow Transplantation

KW - Carbon Monoxide/pharmacology

KW - Cell Differentiation/drug effects

KW - Cells, Cultured

KW - Disease Models, Animal

KW - Heme Oxygenase-1/genetics

KW - Kinetics

KW - Male

KW - Membrane Proteins/genetics

KW - Mice, Inbred BALB C

KW - Mice, Inbred C57BL

KW - Mice, Knockout

KW - Muscle, Smooth, Vascular/drug effects

KW - Myocytes, Smooth Muscle/drug effects

KW - Neointima

KW - Receptor, Platelet-Derived Growth Factor beta/metabolism

KW - Stem Cells/drug effects

KW - Transplantation Chimera

KW - Vascular Remodeling/drug effects

U2 - 10.1161/ATVBAHA.120.315558

DO - 10.1161/ATVBAHA.120.315558

M3 - SCORING: Journal article

C2 - 33853347

VL - 41

SP - 1915

EP - 1927

JO - ARTERIOSCL THROM VAS

JF - ARTERIOSCL THROM VAS

SN - 1079-5642

IS - 6

ER -