ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014
Protein kinase C-δ mediates sepsis-induced activation of complement 5a and urokinase-type plasminogen activator signaling in macrophages.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- Platelets regulate ischemia-induced revascularization and angiogenesis by secretion of growth factor-modulating factors.Blood advances · 2023Article
- Plasminogen System in the Pathophysiology of Sepsis: Upcoming Biomarkers.International journal of molecular sciences · 2023Review
- Targeting Common Signaling Pathways for the Treatment of Stroke and Alzheimer's: a Comprehensive Review.Neurotoxicity research · 2021Review
- Therapeutics targeting the fibrinolytic system.Experimental & molecular medicine · 2020Review
- Quercetin Has Antimetastatic Effects on Gastric Cancer Cells via the Interruption of uPA/uPAR Function by Modulating NF-κb, PKC-δ, ERK1/2, and AMPKα.Integrative cancer therapies · 2018Article
- Urokinase plasminogen activator and receptor promote collagen-induced arthritis through expression in hematopoietic cells.Blood advances · 2017Article
- Common mechanisms of Alzheimer's disease and ischemic stroke: the role of protein kinase C in the progression of age-related neurodegeneration.Journal of Alzheimer's disease : JAD · 2015Review
- Activated Complement Factors as Disease Markers for Sepsis.Disease markers · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
OBJECTIVE AND
designActivations of the complement C5a (C5a) and the urokinase-type plasminogen activator (uPA) are commonly seen together during sepsis. However, the mechanism linking these two important pathways remains elusive. MATERIAL, METHODS AND TREATMENT: We used the C57BL/6 J mice model of sepsis induced by cecal ligation puncture (CLP) procedure, injected anti-C5aR or rottlerin through the tail vein to neutralize C5aR or PKC-δ, and then isolated peritoneal macrophages. Total RNA was isolated from the cells and analyzed by quantitative PCR.
resultsOur study revealed that neutralizing C5aR markedly inhibited sepsis-induced uPA receptor (uPAR) expression and its downstream signaling in macrophage. Similarly, neutralizing uPAR suppressed sepsis activation of C5a signaling. Importantly, inhibition of PKC-δ largely blocked sepsis-induced expression of C5aR and uPAR.
conclusionsOur study demonstrates a crosstalk between the complement C5a signaling and the fibrinolytic uPA pathways, which may depend on each other to maintain their expression and signaling, and reveals a central role of PKC-δ in mediating sepsis-induced activation of these pathways.
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