C1q induces a rapid up-regulation of P-selectin and modulates collagen- and collagen-related peptide-triggered activation in human platelets

Skoglund, Camilla; Wetterö, Jonas; Tengvall, Pentti; Bengtsson, Torbjörn

doi:10.1016/j.imbio.2009.11.004

Cited by 22 publications

(20 citation statements)

References 59 publications

(59 reference statements)

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“…In the same study we also observed that subsequent collagen or collagen-related peptide (GPVI specific)-induced activation of platelets was markedly inhibited [12]. Since the structure of C1q resembles that of collagen and C1q is described to bind to the collagen receptor ␣II␤I on mast cells [11] one may hypothesize that C1q exerts its inhibitory effects on collagen activation via binding to ␣II␤I, or GPVI.…”

Section: Discussionmentioning

confidence: 59%

“…P-selectin is often used as a marker of platelet activation and increased levels of both membrane-bound and soluble P-selectin have been reported during for example stroke, coronary artery disease and diabetes, reviewed in [31]. In a previous study, we speculated that the rapid and transient, but moderate up-regulation of P-selectin on the platelet surface caused by C1q was associated with shedding of the P-selectin molecule, leading to increased levels of soluble P-selectin in plasma [12]. This does not seem to be the case in a whole blood system as C1q per se did not increase the levels of soluble P-selectin.…”

Section: Discussionmentioning

confidence: 96%

“…We and others have previously studied the effects of C1q on isolated cells in suspension [23,12]. In the present study, we have used a whole blood system in an effort to further evaluate the cellular effects of C1q in a more complex experimental setting.…”

Section: Discussionmentioning

confidence: 99%

“…However, in our previous studies, an antibody directed towards the ␣2␤1-integrin did not inhibit the rapid, moderate and transient C1q-induced up-regulation of P-selectin (CD62P) on the platelet surface, whereas an antibody towards the gC1qR showed inhibitory effects. Interestingly, a short pre-incubation with C1q also diminished a subsequent collagen and collagen-related peptide induced platelet activation [12]. Since the collagen-related peptide is described to be selective for GPVI [13], this implies a role for GPVI in C1q-regulated collagen activation of platelets.…”

Section: Introductionmentioning

confidence: 94%

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C1q regulates collagen-dependent production of reactive oxygen species, aggregation and levels of soluble P-selectin in whole blood

2012

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

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C1q regulates collagen-dependent production of reactive oxygen species, aggregation and levels of soluble P-selectin in whole blood

2012

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“…Activation of platelets with potent agonists, including thrombin and arachidonic acid, promotes activation of the alternative complement pathway mediated via binding of C3b to P-selectin [131, 134]. C1q interaction with platelets has also been shown to induce expression of P-selectin on the platelet surface to potentially enhance complement activation via the alternative pathway [135]. C1q interaction with platelets also reduces collagen-mediated platelet activation via GPVI and platelet-neutrophil aggregate formation, a process dependent upon P-selectin interaction with PSGL-1 [77], suggesting a negative feedback on collagen-mediated platelet adhesion to potentially favour enhanced complement activation.…”

Section: The Complement System and Cardiovascular Diseasementioning

confidence: 99%

Complement Activation: An Emerging Player in the Pathogenesis of Cardiovascular Disease

Carter

2012

Scientifica

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A wealth of evidence indicates a fundamental role for inflammation in the pathogenesis of cardiovascular disease (CVD), contributing to the development and progression of atherosclerotic lesion formation, plaque rupture, and thrombosis. An increasing body of evidence supports a functional role for complement activation in the pathogenesis of CVD through pleiotropic effects on endothelial and haematopoietic cell function and haemostasis. Prospective and case control studies have reported strong relationships between several complement components and cardiovascular outcomes, and in vitro studies and animal models support a functional effect. Complement activation, in particular, generation of C5a and C5b-9, influences many processes involved in the development and progression of atherosclerosis, including promotion of endothelial cell activation, leukocyte infiltration into the extracellular matrix, stimulation of cytokine release from vascular smooth muscle cells, and promotion of plaque rupture. Complement activation also influences thrombosis, involving components of the mannose-binding lectin pathway, and C5b-9 in particular, through activation of platelets, promotion of fibrin formation, and impairment of fibrinolysis. The participation of the complement system in inflammation and thrombosis is consistent with the physiological role of the complement system as a rapid effector system conferring protection following vessel injury. However, in the context of CVD, these same processes contribute to development of atherosclerosis, plaque rupture, and thrombosis.

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Interactions between coagulation and complement—their role in inflammation

et al. 2011

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The parallel expression of activation products of the coagulation, fibrinolysis, and complement systems has long been observed in both clinical and experimental settings. Several interconnections between the individual components of these cascades have also been described, and the list of shared regulators is expanding. The coexistence and interplay of hemostatic and inflammatory mediators in the same microenvironment typically ensures a successful host immune defense in compromised barrier settings. However, dysregulation of the cascade activities or functions of inhibitors in one or both systems can result in clinical manifestations of disease, such as sepsis, systemic lupus erythematosus, or ischemia–reperfusion injury, with critical thrombotic and/or inflammatory complications. An appreciation of the precise relationship between complement activation and thrombosis may facilitate the development of novel therapeutics, as well as improve the clinical management of patients with thrombotic conditions that are characterized by complement-associated inflammatory responses.

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C1q induces a rapid up-regulation of P-selectin and modulates collagen- and collagen-related peptide-triggered activation in human platelets

Cited by 22 publications

References 59 publications

C1q regulates collagen-dependent production of reactive oxygen species, aggregation and levels of soluble P-selectin in whole blood

C1q regulates collagen-dependent production of reactive oxygen species, aggregation and levels of soluble P-selectin in whole blood

Complement Activation: An Emerging Player in the Pathogenesis of Cardiovascular Disease

Interactions between coagulation and complement—their role in inflammation

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