ArticleThe Biochemical journal1998
C1q-mediated chemotaxis by human neutrophils: involvement of gClqR and G-protein signalling mechanisms.
Article in The Biochemical journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- Complement in Human Brain Health: Potential of Dietary Food in Relation to Neurodegenerative Diseases.Foods (Basel, Switzerland) · 2023Review
- Unraveling the Relevance of Tissue-Specific Decellularized Extracellular Matrix Hydrogels for Vocal Fold Regenerative Biomaterials: A Comprehensive Proteomic and In Vitro Study.Advanced nanobiomed research · 2023Article
- Article
- Baicalin Targets HSP70/90 to Regulate PKR/PI3K/AKT/eNOS Signaling Pathways.Molecules (Basel, Switzerland) · 2022Article
- Neutrophils: Many Ways to Die.Frontiers in immunology · 2021Review
- Article
- Viral Evasion of the Complement System and Its Importance for Vaccines and Therapeutics.Frontiers in immunology · 2020Review
- Emerging Roles of Complement Protein C1q in Neurodegeneration.Aging and disease · 2019Review
- Systematic Multiomics Analysis of Alterations in C1QBP mRNA Expression and Relevance for Clinical Outcomes in Cancers.Journal of clinical medicine · 2019Article
- Calreticulin contributes to C1q-dependent recruitment of microglia in the leech Hirudo medicinalis following a CNS injury.Medical science monitor : international medical journal of experimental and clinical research · 2014Article
- Oxytocin ameliorates the immediate myocardial injury in heart transplant through down regulation of the neutrophil dependent myocardial apoptosis.Heart views : the official journal of the Gulf Heart Association · 2014Article
- Soluble gC1qR is an autocrine signal that induces B1R expression on endothelial cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Apoptosis amelioration through hypothermic reperfusion in heart transplant.Journal of pharmacology & pharmacotherapeutics · 2013Article
- The leech nervous system: a valuable model to study the microglia involvement in regenerative processes.Clinical & developmental immunology · 2013Review
- The C1q family of proteins: insights into the emerging non-traditional functions.Frontiers in immunology · 2012Article
- Interaction of HmC1q with leech microglial cells: involvement of C1qBP-related molecule in the induction of cell chemotaxis.Journal of neuroinflammation · 2012Article
- Complement C1q enhances homing-related responses of hematopoietic stem/progenitor cells.Transfusion · 2010Article
- C1q, the recognition subcomponent of the classical pathway of complement, drives microglial activation.Journal of neuroscience research · 2009Article
- Deficiency in complement C1q improves histological and functional locomotor outcome after spinal cord injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Cathepsin g is required for sustained inflammation and tissue injury after reperfusion of ischemic kidneys.The American journal of pathology · 2007Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1q, the first component of the classical pathway of the complement system, interacts with various cell types and triggers a variety of cell-specific cellular responses, such as oxidative burst, chemotaxis, phagocytosis, etc. Different biological responses are attributed to the interaction of C1q with more than one putative cell-surface C1q receptor/C1q-binding protein. Previously, it has been shown that C1q-mediated oxidative burst by neutrophils is not linked to G-protein-coupled fMet-Leu-Phe-mediated response. In the present study, we have investigated neutrophil migration brought about by C1q and tried to identify the signal-transduction pathways involved in the chemotactic response. We found that C1q stimulated neutrophil migration in a dose-dependent manner, primarily by enhancing chemotaxis (directed movement) rather than chemokinesis (random movement). This C1q-induced chemotaxis could be abolished by an inhibitor of G-proteins (pertussis toxin) and PtdIns(3,4,5)P3 kinase (wortmannin and LY294002). The collagen tail of C1q appeared to mediate chemotaxis. gC1qR, a C1q-binding protein, has recently been reported to participate in C1q-mediated chemotaxis of murine mast cells and human eosinophils. We observed that gC1qR enhanced binding of free C1q to adherent neutrophils and promoted C1q-mediated chemotaxis of neutrophils by nearly seven-fold. Our results suggests C1q-mediated chemotaxis involves gC1qR as well as G-protein-coupled signal-transduction mechanisms operating downstream to neutrophil chemotaxis.
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