Circulating BMP9 Protects the Pulmonary Endothelium during Inflammation-induced Lung Injury in Mice

Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome. Circulating BMP9 (bone morphogenetic protein 9) is emerging as an important regulator of pulmonary vascular homeostasis. To determine whether endogenous BMP...

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Published inAmerican journal of respiratory and critical care medicine Vol. 203; no. 11; pp. 1419 - 1430
Main Authors Li, Wei, Long, Lu, Yang, Xudong, Tong, Zhen, Southwood, Mark, King, Ross, Caruso, Paola, Upton, Paul D, Yang, Peiran, Bocobo, Geoffrey A, Nikolic, Ivana, Higuera, Angelica, Salmon, Richard M, Jiang, He, Lodge, Katharine M, Hoenderdos, Kim, Baron, Rebecca M, Yu, Paul B, Condliffe, Alison M, Summers, Charlotte, Nourshargh, Sussan, Chilvers, Edwin R, Morrell, Nicholas W
Format Journal Article
LanguageEnglish
Published United States American Thoracic Society 01.06.2021
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Abstract Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome. Circulating BMP9 (bone morphogenetic protein 9) is emerging as an important regulator of pulmonary vascular homeostasis. To determine whether endogenous BMP9 plays a role in preserving pulmonary endothelial integrity and whether loss of endogenous BMP9 occurs during LPS challenge. A BMP9-neutralizing antibody was administrated to healthy adult mice, and lung vasculature was examined. Potential mechanisms were delineated by transcript analysis in human lung endothelial cells. The impact of BMP9 administration was evaluated in a murine acute lung injury model induced by inhaled LPS. Levels of BMP9 were measured in plasma from patients with sepsis and from endotoxemic mice. Subacute neutralization of endogenous BMP9 in mice (  = 12) resulted in increased lung vascular permeability (  = 0.022), interstitial edema (  = 0.0047), and neutrophil extravasation (  = 0.029) compared with IgG control treatment (  = 6). In pulmonary endothelial cells, BMP9 regulated transcriptome pathways implicated in vascular permeability and cell-membrane integrity. Augmentation of BMP9 signaling in mice (  = 8) prevented inhaled LPS-induced lung injury (  = 0.0027) and edema (  < 0.0001). In endotoxemic mice (  = 12), endogenous circulating BMP9 concentrations were markedly reduced, the causes of which include a transient reduction in hepatic BMP9 mRNA expression and increased elastase activity in plasma. In human patients with sepsis (  = 10), circulating concentratons of BMP9 were also markedly reduced (  < 0.0001). Endogenous circulating BMP9 is a pulmonary endothelial-protective factor, downregulated during inflammation. Exogenous BMP9 offers a potential therapy to prevent increased pulmonary endothelial permeability in lung injury.
AbstractList Rationale: Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome. Circulating BMP9 (bone morphogenetic protein 9) is emerging as an important regulator of pulmonary vascular homeostasis. Objectives:To determine whether endogenous BMP9 plays a role in preserving pulmonary endothelial integrity and whether loss of endogenous BMP9 occurs during LPS challenge. Methods: A BMP9-neutralizing antibody was administrated to healthy adult mice, and lung vasculature was examined. Potential mechanisms were delineated by transcript analysis in human lung endothelial cells. The impact of BMP9 administration was evaluated in a murine acute lung injury model induced by inhaled LPS. Levels of BMP9 were measured in plasma from patients with sepsis and from endotoxemic mice. Measurements and Main Results: Subacute neutralization of endogenous BMP9 in mice (N = 12) resulted in increased lung vascular permeability (P = 0.022), interstitial edema (P = 0.0047), and neutrophil extravasation (P = 0.029) compared with IgG control treatment (N = 6). In pulmonary endothelial cells, BMP9 regulated transcriptome pathways implicated in vascular permeability and cell-membrane integrity. Augmentation of BMP9 signaling in mice (N = 8) prevented inhaled LPS-induced lung injury (P = 0.0027) and edema (P < 0.0001). In endotoxemic mice (N = 12), endogenous circulating BMP9 concentrations were markedly reduced, the causes of which include a transient reduction in hepatic BMP9 mRNA expression and increased elastase activity in plasma. In human patients with sepsis (N = 10), circulating concentratons of BMP9 were also markedly reduced (P < 0.0001). Conclusions: Endogenous circulating BMP9 is a pulmonary endothelial-protective factor, downregulated during inflammation. Exogenous BMP9 offers a potential therapy to prevent increased pulmonary endothelial permeability in lung injury.
Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome. Circulating BMP9 (bone morphogenetic protein 9) is emerging as an important regulator of pulmonary vascular homeostasis. This study is aimed to determine whether endogenous BMP9 plays a role in preserving pulmonary endothelial integrity and whether loss of endogenous BMP9 occurs during LPS challenge. The result of the study conclude that endogenous circulating BMP9 is a pulmonary endothelial-protective factor, downregulated during inflammation. Exogenous BMP9 offers a potential therapy to prevent increased pulmonary endothelial permeability in lung injury.
Rationale: Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome. Circulating BMP9 (bone morphogenetic protein 9) is emerging as an important regulator of pulmonary vascular homeostasis. Objectives: To determine whether endogenous BMP9 plays a role in preserving pulmonary endothelial integrity and whether loss of endogenous BMP9 occurs during LPS challenge. Methods: A BMP9-neutralizing antibody was administrated to healthy adult mice, and lung vasculature was examined. Potential mechanisms were delineated by transcript analysis in human lung endothelial cells. The impact of BMP9 administration was evaluated in a murine acute lung injury model induced by inhaled LPS. Levels of BMP9 were measured in plasma from patients with sepsis and from endotoxemic mice. Measurements and Main Results: Subacute neutralization of endogenous BMP9 in mice ( N  = 12) resulted in increased lung vascular permeability ( P  = 0.022), interstitial edema ( P  = 0.0047), and neutrophil extravasation ( P  = 0.029) compared with IgG control treatment ( N  = 6). In pulmonary endothelial cells, BMP9 regulated transcriptome pathways implicated in vascular permeability and cell-membrane integrity. Augmentation of BMP9 signaling in mice ( N  = 8) prevented inhaled LPS–induced lung injury ( P  = 0.0027) and edema ( P  < 0.0001). In endotoxemic mice ( N  = 12), endogenous circulating BMP9 concentrations were markedly reduced, the causes of which include a transient reduction in hepatic BMP9 mRNA expression and increased elastase activity in plasma. In human patients with sepsis ( N  = 10), circulating concentratons of BMP9 were also markedly reduced ( P  < 0.0001). Conclusions: Endogenous circulating BMP9 is a pulmonary endothelial-protective factor, downregulated during inflammation. Exogenous BMP9 offers a potential therapy to prevent increased pulmonary endothelial permeability in lung injury.
Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome. Circulating BMP9 (bone morphogenetic protein 9) is emerging as an important regulator of pulmonary vascular homeostasis. To determine whether endogenous BMP9 plays a role in preserving pulmonary endothelial integrity and whether loss of endogenous BMP9 occurs during LPS challenge. A BMP9-neutralizing antibody was administrated to healthy adult mice, and lung vasculature was examined. Potential mechanisms were delineated by transcript analysis in human lung endothelial cells. The impact of BMP9 administration was evaluated in a murine acute lung injury model induced by inhaled LPS. Levels of BMP9 were measured in plasma from patients with sepsis and from endotoxemic mice. Subacute neutralization of endogenous BMP9 in mice (  = 12) resulted in increased lung vascular permeability (  = 0.022), interstitial edema (  = 0.0047), and neutrophil extravasation (  = 0.029) compared with IgG control treatment (  = 6). In pulmonary endothelial cells, BMP9 regulated transcriptome pathways implicated in vascular permeability and cell-membrane integrity. Augmentation of BMP9 signaling in mice (  = 8) prevented inhaled LPS-induced lung injury (  = 0.0027) and edema (  < 0.0001). In endotoxemic mice (  = 12), endogenous circulating BMP9 concentrations were markedly reduced, the causes of which include a transient reduction in hepatic BMP9 mRNA expression and increased elastase activity in plasma. In human patients with sepsis (  = 10), circulating concentratons of BMP9 were also markedly reduced (  < 0.0001). Endogenous circulating BMP9 is a pulmonary endothelial-protective factor, downregulated during inflammation. Exogenous BMP9 offers a potential therapy to prevent increased pulmonary endothelial permeability in lung injury.
Author Yang, Peiran
Yu, Paul B
Morrell, Nicholas W
Hoenderdos, Kim
Caruso, Paola
Li, Wei
Nikolic, Ivana
Southwood, Mark
Salmon, Richard M
Yang, Xudong
Baron, Rebecca M
Chilvers, Edwin R
Nourshargh, Sussan
Tong, Zhen
Bocobo, Geoffrey A
Jiang, He
Long, Lu
Condliffe, Alison M
Lodge, Katharine M
Summers, Charlotte
Upton, Paul D
King, Ross
Higuera, Angelica
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ContentType Journal Article
Copyright Copyright American Thoracic Society Jun 1, 2021
Copyright © 2021 by the American Thoracic Society 2021
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Issue 11
Keywords BMP signaling in endothelial cells
BMP9
lung injury
pulmonary endothelium
Language English
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Snippet Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome. Circulating...
Rationale: Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome....
Rationale: Pulmonary endothelial permeability contributes to the high-permeability pulmonary edema that characterizes acute respiratory distress syndrome....
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StartPage 1419
SubjectTerms Acute Lung Injury - blood
Acute Lung Injury - etiology
Acute Lung Injury - pathology
Animals
Case-Control Studies
Chronic obstructive pulmonary disease
Endothelial Cells - metabolism
Endothelium - pathology
Endotoxemia - blood
Endotoxemia - etiology
Endotoxemia - pathology
Female
Growth Differentiation Factor 2 - blood
Humans
Lung diseases
Male
Mice
Original
Pulmonary Edema - blood
Pulmonary Edema - etiology
Pulmonary Edema - pathology
Pulmonary hypertension
Respiratory diseases
Respiratory distress syndrome
Sepsis - blood
Sepsis - etiology
Sepsis - pathology
Title Circulating BMP9 Protects the Pulmonary Endothelium during Inflammation-induced Lung Injury in Mice
URI https://www.ncbi.nlm.nih.gov/pubmed/33320799
https://www.proquest.com/docview/2543869538
https://search.proquest.com/docview/2470629128
https://pubmed.ncbi.nlm.nih.gov/PMC8456542
Volume 203
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