What question did this study set out to answer?

To investigate whether PCTR1 protects against lipopolysaccharide-induced pulmonary endothelial glycocalyx degradation and to delineate the underlying molecular mechanisms.

July 3, 2021Respiratory ResearchOpen Access

Protectin conjugates in tissue regeneration 1 restores lipopolysaccharide-induced pulmonary endothelial glycocalyx loss via ALX/SIRT1/NF-kappa B axis

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Authors

XWXinyang WangTianjin University of Science and Technology XLXinyu LiZhengzhou University CWChenghua WuWannan Medical College

Discussion

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Implication

Preclinical study demonstrates that PCTR1 restores pulmonary endothelial glycocalyx in LPS-induced sepsis models, suggesting a novel therapeutic pathway for acute lung injury.

Key Points

To investigate whether PCTR1 protects against lipopolysaccharide-induced pulmonary endothelial glycocalyx degradation and to delineate the underlying molecular mechanisms.
Administered 100 ng/mouse of PCTR1 intraperitoneally after lipopolysaccharide challenge to assess survival, pulmonary function, and lung inflammation.
Evaluated endothelial glycocalyx integrity and shedding markers using immunofluorescence, Western blot, and ELISA in mice and human umbilical vein endothelial cells treated with pathway inhibitors (BOC-2, EX527, and BAY11-7082).
PCTR1 increased survival, improved lung function, and decreased lung inflammation along with systemic levels of TNF-α, IL-6, and IL-1β in mice with LPS-induced sepsis.
PCTR1 preserved glycocalyx structure, reduced serum heparin sulphate, syndecan-1, and hyaluronic acid, downregulated heparanase expression, and upregulated exostosin-1.
Glycocalyx restoration by PCTR1 was blocked by the ALX antagonist BOC-2 and the SIRT1 inhibitor EX527, while NF-κB inhibition with BAY11-7082 prevented LPS-induced glycocalyx loss.

Cite This Study

Wang et al. (2021) studied this question.

synapsesocial.com/papers/6a9edf3c0fc97ef28e11f936 https://doi.org/10.1186/s12931-021-01793-x

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July 3, 2021Respiratory ResearchOpen Access

Protectin conjugates in tissue regeneration 1 restores lipopolysaccharide-induced pulmonary endothelial glycocalyx loss via ALX/SIRT1/NF-kappa B axis

View Full Paper

Ask AI

Bookmark

Authors

XWXinyang WangTianjin University of Science and Technology XLXinyu LiZhengzhou University CWChenghua WuWannan Medical College

Discussion

Member takes

Implication

Preclinical study demonstrates that PCTR1 restores pulmonary endothelial glycocalyx in LPS-induced sepsis models, suggesting a novel therapeutic pathway for acute lung injury.

Key Points

To investigate whether PCTR1 protects against lipopolysaccharide-induced pulmonary endothelial glycocalyx degradation and to delineate the underlying molecular mechanisms.
Administered 100 ng/mouse of PCTR1 intraperitoneally after lipopolysaccharide challenge to assess survival, pulmonary function, and lung inflammation.
Evaluated endothelial glycocalyx integrity and shedding markers using immunofluorescence, Western blot, and ELISA in mice and human umbilical vein endothelial cells treated with pathway inhibitors (BOC-2, EX527, and BAY11-7082).
PCTR1 increased survival, improved lung function, and decreased lung inflammation along with systemic levels of TNF-α, IL-6, and IL-1β in mice with LPS-induced sepsis.
PCTR1 preserved glycocalyx structure, reduced serum heparin sulphate, syndecan-1, and hyaluronic acid, downregulated heparanase expression, and upregulated exostosin-1.
Glycocalyx restoration by PCTR1 was blocked by the ALX antagonist BOC-2 and the SIRT1 inhibitor EX527, while NF-κB inhibition with BAY11-7082 prevented LPS-induced glycocalyx loss.

Cite This Study

Wang et al. (2021) studied this question.

synapsesocial.com/papers/6a9edf3c0fc97ef28e11f936 https://doi.org/10.1186/s12931-021-01793-x

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