Role of NF-κB Pathway on Platelet Activation

Schattner, Mirta

doi:10.1161/circresaha.113.302333

Cited by 11 publications

(16 citation statements)

References 12 publications

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“…We agree with Dr Schattner 1 that there is evidence in recent published reports for both positive and negative modulation of specific platelet activation responses by NF-κB signaling. The example that we cited 2 describes a previously unrecognized negative feedback mechanism for fine-tuning of integrin α IIb β 3 activation and aggregation of stimulated platelets by NF-κB–dependent signaling.…”

supporting

confidence: 90%

“…We appreciate Dr Schattner's letter 1 and comments on our recent review in Circulation Research 2 outlining facets of platelets as effectors of inflammation in vascular diseases. Unfortunately, we did not have space for an in-depth discussion of all aspects of noncanonical and nongenomic activities of the nuclear family kappa B (NF-κB) pathway in these cells.…”

mentioning

confidence: 99%

“…One of these was the review of transcription factors in anucleate platelets by Spinelli et al, 3 mentioned in Dr Schattner's letter. 1 The Spinelli review 3 cites several reports mentioned by Dr Schattner 1 that we did not include in our review because of space limitations.…”

mentioning

confidence: 99%

“…4 Spinelli et al also interpreted these observations 4 in this fashion and discussed them in this context. 3 Based on reports cited by Schattner 1 and Spinelli et al, 3 several of which involve inhibitors that block the NF-κB pathway in other cell types, there may also be positive NF-κB–dependent signaling in activated platelets depending on the functional response(s) assayed and the experimental conditions chosen. Spinelli et al 3 commented that additional work and a variety of experimental approaches will be required to fully characterize noncanonical activities of molecular members of the NF-κB pathway in activated platelets.…”

mentioning

confidence: 99%

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Rondina¹,

Weyrich²,

Zimmerman

2013

Circulation Research

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supporting

confidence: 90%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Rondina¹,

Weyrich²,

Zimmerman

2013

Circulation Research

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“…The upregulation of CRP also increases tissue factor production, activating the extrinsic blood coagulation pathway. Increased adhesion of macrophages upregulates transcription factor NF-κB, and it has recently been identified that NF-κB plays a substantial role in the enhancement of platelet aggregation [43]. The upregulation of activated NF-κB furthermore leads to increased smooth muscle and vascular cell inflammation through the increase of cytokines like IL-6 [13].…”

Section: Macrophage Activationmentioning

confidence: 99%

Oxidative stress biomarkers in type 2 diabetes mellitus for assessment of cardiovascular disease risk

Robson

Kundur

Singh

2018

Diabetes & Metabolic Syndrome: Clinical Research & Revi

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Stress-induced modulation of NF-κB activation, inflammation-associated gene expression, and cytokine levels in blood of healthy men

Kuebler

Zuccarella-Hackl

Arpagaus

et al. 2015

Brain, Behavior, and Immunity

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Acute psychosocial stress stimulates transient increases in circulating pro-inflammatory plasma cytokines, but little is known about stress effects on anti-inflammatory cytokines or underlying mechanisms. We investigated the stress kinetics and interrelations of pro- and anti-inflammatory measures on the transcriptional and protein level. Forty-five healthy men were randomly assigned to either a stress or control group. While the stress group underwent an acute psychosocial stress task, the second group participated in a non-stress control condition. We repeatedly measured before and up to 120min after stress DNA binding activity of the pro-inflammatory transcription factor NF-κB (NF-κB-BA) in peripheral blood mononuclear cells, whole-blood mRNA levels of NF-κB, its inhibitor IκBα, and of the pro-inflammatory cytokines interleukin (IL)-1ß and IL-6, and the anti-inflammatory cytokine IL-10. We also repeatedly measured plasma levels of IL-1ß, IL-6, and IL-10. Compared to non-stress, acute stress induced significant and rapid increases in NF-κB-BA and delayed increases in plasma IL-6 and mRNA of IL-1ß, IL-6, and IκBα (p's<.045). In the stress group, significant increases over time were also observed for NF-κB mRNA and plasma IL-1ß and IL-10 (p's<.055). NF-κB-BA correlated significantly with mRNA of IL-1β (r=.52, p=.002), NF-κB (r=.48, p=.004), and IκBα (r=.42, p=.013), and marginally with IL-6 mRNA (r=.31, p=.11). Plasma cytokines did not relate to NF-κB-BA or mRNA levels of the respective cytokines. Our data suggest that stress induces increases in NF-κB-BA that relate to subsequent mRNA expression of pro-inflammatory, but not anti-inflammatory cytokines, and of regulatory-cytoplasmic-proteins. The stress-induced increases in plasma cytokines do not seem to derive from de novo synthesis in circulating blood cells.

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Role of NF-κB Pathway on Platelet Activation

Cited by 11 publications

References 12 publications

Reply to Schattner

Reply to Schattner

Oxidative stress biomarkers in type 2 diabetes mellitus for assessment of cardiovascular disease risk

Stress-induced modulation of NF-κB activation, inflammation-associated gene expression, and cytokine levels in blood of healthy men

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