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C1q regulates collagen-dependent production of reactive oxygen species, aggregation and levels of soluble P-selectin in whole blood
Linköping University, Department of Medical and Health Sciences, Pharmacology. Linköping University, Faculty of Health Sciences. Linköping University, Department of Physics, Chemistry and Biology, Molecular Surface Physics and Nano Science.
Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences.ORCID iD: 0000-0002-6916-5490
University of Örebro.
2012 (English)In: Immunology Letters, ISSN 0165-2478, E-ISSN 1879-0542, Vol. 142, no 1-2, 28-33 p.Article in journal (Refereed) Published
Abstract [en]

Blood platelets express several receptors involved in immunity (e.g. complement-, toll-like- and Fc gamma-receptors) and release inflammatory mediators. Furthermore, formation of platelet-leukocyte aggregates has an important role during inflammatory conditions such as coronary artery disease. Thus, apart from their well-known role in haemostasis, platelets are today also recognized as cells with immunomodulatory properties. less thanbrgreater than less thanbrgreater thanWe have previously reported regulatory effects of complement protein 1q (C1q) on platelet activation in experimental setups using isolated cells. In the present study we have proceeded by investigating effects of C1q on collagen-induced aggregation, production of reactive oxygen species (ROS), formation of platelet-leukocyte aggregates and levels of soluble P-selectin in whole blood. less thanbrgreater than less thanbrgreater thanImpedance measurements showed that C1q inhibited collagen-induced aggregation whereas it potentiated the collagen-provoked production of ROS in a luminol-dependent chemiluminescence assay. The effects of C1q on aggregation and ROS-production were dependent upon platelets, as they were no longer observed in presence of the platelet (GpIIb/IIIa) inhibitor Reopro. Furthermore, the levels of soluble P-selectin were found to be lowered upon treatment with C1q prior to addition of collagen. There was also a trend towards a decreased formation of large platelet-leukocyte aggregates in collagen-stimulated whole blood following C1q treatment. In conclusion, our data indicate that C1q could have a role in regulating platelet activation and associated leukocyte recruitment during vessel wall injury. This has implications for inflammatory disorders such as coronary artery disease.

Place, publisher, year, edition, pages
Elsevier , 2012. Vol. 142, no 1-2, 28-33 p.
Keyword [en]
C1q, Collagen, Platelet, Platelet-leukocyte aggregate, Reactive oxygen species, Whole blood
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-76534DOI: 10.1016/j.imlet.2011.11.003ISI: 000301683800004OAI: diva2:515133

Funding Agencies|strategic research area "Materials in Medicine"||County Council of Ostergotland||Swedish Research Council||Heart and Lung Foundation||Swedish Society of Medicine||Swedish Fund for Research Without Animal Experiments||Eleanora Demoroutis||Nanna Svartz foundation||Magn. Bergvall foundation||Lars Hiertas foundation||Goljes research foundation||

Available from: 2012-04-12 Created: 2012-04-11 Last updated: 2015-06-29

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Skoglund, CarolineWetterö, Jonas
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PharmacologyFaculty of Health SciencesMolecular Surface Physics and Nano ScienceRheumatology
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