ArticleThe Journal of biological chemistry2015
C1q Deficiency Promotes Pulmonary Vascular Inflammation and Enhances the Susceptibility of the Lung Endothelium to Injury.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Integrative bioinformatics reveals complement dysregulation: critical insights into C1q, C1r, and C1s in aortic dissection pathogenesis.Molecular genetics and genomics : MGG · 2026Article
- Complement protein C1q induces endothelial apoptosis through C1qBP regulation of mitochondrial function in lung endothelial cells in systemic sclerosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Severe pulmonary involvement and elevated interferon-stimulated genes expression in two siblings with a novelJournal of human immunity · 2026Article
- Protective Effect of Low 2-O, 3-O Desulfated Heparin (ODSH) Against LPS-Induced Acute Lung Injury in Mice.Biomolecules · 2025Article
- Rutin alleviates ventilator-induced lung injury by inhibiting NLRP3 inflammasome activation.iScience · 2023Article
- Article
- Efferocytosis of vascular cells in cardiovascular disease.Pharmacology & therapeutics · 2022Review
- Association of Serum Complement C1q and C3 Level with Age-Related Macular Degeneration in Women.Journal of inflammation research · 2022Article
- Functional heterogeneity of alveolar macrophage population based on expression of CXCL2.Science immunology · 2020Article
- Adiponectin deficiency induces mitochondrial dysfunction and promotes endothelial activation and pulmonary vascular injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- TREM-1 Attenuates RIPK3-mediated Necroptosis in Hyperoxia-induced Lung Injury in Neonatal Mice.American journal of respiratory cell and molecular biology · 2019Article
- A simple protocol for isolating mouse lung endothelial cells.Scientific reports · 2019Article
- Anti inflammatory effect of asiaticoside on human umbilical vein endothelial cells induced by ox-LDL.Cytotechnology · 2018Article
- Obesity-Induced Endoplasmic Reticulum Stress Causes Lung Endothelial Dysfunction and Promotes Acute Lung Injury.American journal of respiratory cell and molecular biology · 2017Article
- Pericytes and immune cells contribute to complement activation in tubulointerstitial fibrosis.American journal of physiology. Renal physiology · 2017Article
- Increased Circulating Endothelial Microparticles Associated with PAK4 Play a Key Role in Ventilation-Induced Lung Injury Process.BioMed research international · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
The collectin proteins are innate immune molecules found in high concentrations on the epithelial and endothelial surfaces of the lung. While these proteins are known to have important anti-inflammatory actions in the airways of the lung little is known of their functional importance in the pulmonary circulation. We recently demonstrated that the circulating collectin protein adiponectin has potent anti-inflammatory effects on the lung endothelium, leading us to reason that other structurally related proteins might have similar effects. To test this hypothesis, we investigated the anti-inflammatory actions of C1q in lung endothelial homeostasis and the pulmonary vascular response to LPS or HCl injury. We show that lung endothelium from C1q-deficient (C1q(-/-)) mice expresses higher baseline levels of the vascular adhesion markers ICAM-1, VCAM-1, and E-selectin when compared with wild-type mice. Further, we demonstrate that these changes are associated with enhanced susceptibility of the lung to injury as evident by increased expression of adhesion markers, enhanced production of pro-inflammatory cytokines, and augmented neutrophil recruitment. Additionally, we found that C1q(-/-) mice also exhibited enhanced endothelial barrier dysfunction after injury as manifested by decreased expression of junctional adherens proteins and enhanced vascular leakage. Mechanistically, C1q appears to mediate its effects by inhibiting phosphorylation of p38 mitogen-activated protein kinase (MAPK) and blocking nuclear translocation of the P65 subunit of nuclear factor (NF)-κB. In summary, our findings indicate a previously unrecognized role for C1q in pulmonary vascular homeostasis and provide added support for the hypothesis that circulating collectin proteins have protective effects on the lung endothelium.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.