MCTR1 alleviates lipopolysaccharide-induced acute lung injury by protecting lung endothelial glycocalyx

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MCTR1 alleviates lipopolysaccharide-induced acute lung injury by protecting lung endothelial glycocalyx. / Li, Hui; Hao, Yu; Yang, Li Li; Wang, Xin Yang; Li, Xin Yu; Bhandari, Suwas; Han, Jun; Liu, Yong Jian; Gong, Yu Qiang; Scott, Aaron; Smith, Fang Gao; Jin, Sheng Wei.

In: Journal of Cellular Physiology, 09.02.2020.

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Li, Hui ; Hao, Yu ; Yang, Li Li ; Wang, Xin Yang ; Li, Xin Yu ; Bhandari, Suwas ; Han, Jun ; Liu, Yong Jian ; Gong, Yu Qiang ; Scott, Aaron ; Smith, Fang Gao ; Jin, Sheng Wei. / MCTR1 alleviates lipopolysaccharide-induced acute lung injury by protecting lung endothelial glycocalyx. In: Journal of Cellular Physiology. 2020.

Bibtex

@article{583c30a9566f4f79ad19a2b56267e038,
title = "MCTR1 alleviates lipopolysaccharide-induced acute lung injury by protecting lung endothelial glycocalyx",
abstract = "Endothelial glycocalyx degradation, critical for increased pulmonary vascular permeability, is thought to facilitate the development of sepsis into the multiple organ failure. Maresin conjugates in tissue regeneration 1 (MCTR1), a macrophage-derived lipid mediator, which exhibits potentially beneficial effects via the regulation of bacterial phagocytosis, promotion of inflammation resolution, and regeneration of tissue. In this study, we show that MCTR1 (100 ng/mouse) enhances the survival of mice with lipopolysaccharide (LPS)-induced (15 mg/kg) sepsis. MCTR1 alleviates LPS (10 mg/kg)-induced lung dysfunction and lung tissue inflammatory response by decreasing inflammatory cytokines (tumor necrosis factor-α, interleukin-1β [IL-1β], and IL-6) expression in serum and reducing the serum levels of heparan sulfate (HS) and syndecan-1. In human umbilical vein endothelial cells (HUVECs) experiments, MCTR1 (100 nM) was added to the culture medium with LPS for 6 hr. MCTR1 treatment markedly inhibited HS degradation by downregulating heparanase (HPA) protein expression in vivo and in vitro. Further analyses indicated that MCTR1 upregulates sirtuin 1 (SIRT1) expression and decreases NF-κB p65 phosphorylation. In the presence of BOC-2 or EX527, the above effects of MCTR1 were abolished. These results suggest that MCTR1 protects against LPS-induced sepsis in mice by attenuating pulmonary endothelial glycocalyx injury via the ALX/SIRT1/NF-κB/HPA pathway.",
keywords = "endothelial glycocalyx, HPA, MCTR1, sepsis, SIRT1",
author = "Hui Li and Yu Hao and Yang, {Li Li} and Wang, {Xin Yang} and Li, {Xin Yu} and Suwas Bhandari and Jun Han and Liu, {Yong Jian} and Gong, {Yu Qiang} and Aaron Scott and Smith, {Fang Gao} and Jin, {Sheng Wei}",
note = "{\textcopyright} 2020 Wiley Periodicals, Inc.",
year = "2020",
month = feb,
day = "9",
doi = "10.1002/jcp.29628",
language = "English",
journal = "Journal of Cellular Physiology",
issn = "0021-9541",
publisher = "Wiley",

}

RIS

TY - JOUR

T1 - MCTR1 alleviates lipopolysaccharide-induced acute lung injury by protecting lung endothelial glycocalyx

AU - Li, Hui

AU - Hao, Yu

AU - Yang, Li Li

AU - Wang, Xin Yang

AU - Li, Xin Yu

AU - Bhandari, Suwas

AU - Han, Jun

AU - Liu, Yong Jian

AU - Gong, Yu Qiang

AU - Scott, Aaron

AU - Smith, Fang Gao

AU - Jin, Sheng Wei

N1 - © 2020 Wiley Periodicals, Inc.

PY - 2020/2/9

Y1 - 2020/2/9

N2 - Endothelial glycocalyx degradation, critical for increased pulmonary vascular permeability, is thought to facilitate the development of sepsis into the multiple organ failure. Maresin conjugates in tissue regeneration 1 (MCTR1), a macrophage-derived lipid mediator, which exhibits potentially beneficial effects via the regulation of bacterial phagocytosis, promotion of inflammation resolution, and regeneration of tissue. In this study, we show that MCTR1 (100 ng/mouse) enhances the survival of mice with lipopolysaccharide (LPS)-induced (15 mg/kg) sepsis. MCTR1 alleviates LPS (10 mg/kg)-induced lung dysfunction and lung tissue inflammatory response by decreasing inflammatory cytokines (tumor necrosis factor-α, interleukin-1β [IL-1β], and IL-6) expression in serum and reducing the serum levels of heparan sulfate (HS) and syndecan-1. In human umbilical vein endothelial cells (HUVECs) experiments, MCTR1 (100 nM) was added to the culture medium with LPS for 6 hr. MCTR1 treatment markedly inhibited HS degradation by downregulating heparanase (HPA) protein expression in vivo and in vitro. Further analyses indicated that MCTR1 upregulates sirtuin 1 (SIRT1) expression and decreases NF-κB p65 phosphorylation. In the presence of BOC-2 or EX527, the above effects of MCTR1 were abolished. These results suggest that MCTR1 protects against LPS-induced sepsis in mice by attenuating pulmonary endothelial glycocalyx injury via the ALX/SIRT1/NF-κB/HPA pathway.

AB - Endothelial glycocalyx degradation, critical for increased pulmonary vascular permeability, is thought to facilitate the development of sepsis into the multiple organ failure. Maresin conjugates in tissue regeneration 1 (MCTR1), a macrophage-derived lipid mediator, which exhibits potentially beneficial effects via the regulation of bacterial phagocytosis, promotion of inflammation resolution, and regeneration of tissue. In this study, we show that MCTR1 (100 ng/mouse) enhances the survival of mice with lipopolysaccharide (LPS)-induced (15 mg/kg) sepsis. MCTR1 alleviates LPS (10 mg/kg)-induced lung dysfunction and lung tissue inflammatory response by decreasing inflammatory cytokines (tumor necrosis factor-α, interleukin-1β [IL-1β], and IL-6) expression in serum and reducing the serum levels of heparan sulfate (HS) and syndecan-1. In human umbilical vein endothelial cells (HUVECs) experiments, MCTR1 (100 nM) was added to the culture medium with LPS for 6 hr. MCTR1 treatment markedly inhibited HS degradation by downregulating heparanase (HPA) protein expression in vivo and in vitro. Further analyses indicated that MCTR1 upregulates sirtuin 1 (SIRT1) expression and decreases NF-κB p65 phosphorylation. In the presence of BOC-2 or EX527, the above effects of MCTR1 were abolished. These results suggest that MCTR1 protects against LPS-induced sepsis in mice by attenuating pulmonary endothelial glycocalyx injury via the ALX/SIRT1/NF-κB/HPA pathway.

KW - endothelial glycocalyx

KW - HPA

KW - MCTR1

KW - sepsis

KW - SIRT1

UR - http://www.scopus.com/inward/record.url?scp=85079162008&partnerID=8YFLogxK

U2 - 10.1002/jcp.29628

DO - 10.1002/jcp.29628

M3 - Article

C2 - 32037554

AN - SCOPUS:85079162008

JO - Journal of Cellular Physiology

JF - Journal of Cellular Physiology

SN - 0021-9541

ER -