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C1q regulates collagen-dependent production of reactive oxygen species, aggregation and levels of soluble P-selectin in whole blood
Department of Biomedicine, School of Health and Medical Sciences, Örebro University, Örebro, Sweden; Division of Molecular Surface Physics and Nanoscience, Department of Physics, Chemistry and Biology, Linköping University, Linköping, Sweden.
Rheumatology/Autoimmunity and Immune Regulation Unit (AIR), Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
Örebro universitet, Institutionen för hälsovetenskap och medicin. Department of Biomedicine, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
2012 (engelsk)Inngår i: Immunology Letters, ISSN 0165-2478, E-ISSN 1879-0542, Vol. 142, nr 1-2, s. 28-33Artikkel i tidsskrift (Fagfellevurdert) 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. We 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. Impedance 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.

sted, utgiver, år, opplag, sider
Amsterdam, Netherlands: Elsevier, 2012. Vol. 142, nr 1-2, s. 28-33
Emneord [en]
C1q, collagen, platelet, platelet–leukocyte aggregate, reactive oxygen species, whole blood
HSV kategori
Forskningsprogram
Medicin
Identifikatorer
URN: urn:nbn:se:oru:diva-22496DOI: 10.1016/j.imlet.2011.11.003ISI: 000301683800004PubMedID: 22142906Scopus ID: 2-s2.0-84857192721OAI: oai:DiVA.org:oru-22496DiVA, id: diva2:514674
Forskningsfinansiär
Swedish Heart Lung Foundation
Merknad

Funding Agencies:

strategic research area "Materials in Medicine" 

County Council of Östergötland

 Swedish Research Council 

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 

Tilgjengelig fra: 2012-04-10 Laget: 2012-04-10 Sist oppdatert: 2018-09-11bibliografisk kontrollert

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