Trends in Pharmacological Sciences
The involvement of platelets in non-thrombotic processes
References (34)
- et al.
Immunol. Today
(1986) - et al.
J. Allergy Clin. Immunol.
(1984) - et al.
Lancet
(1985) - et al.
Lancet
(1986) - et al.
J. Allergy Clin. Immunol.
(1986) - et al.
Lancet
(1987) - et al.
Fertil. Steril.
(1987) - et al.
Folia Haematol.
(1979)
Eur. J. Immunol.
Int. Archs Allergy Appl. Immunol.
Eur. J. Respir. Dis.
Agents Actions
Nature
N. Engl. J. Med.
Cited by (66)
Procoagulant State of Sleep Apnea Depends on Systemic Inflammation and Endothelial Damage
2022, Archivos de BronconeumologiaA novel murine model of pulmonary fibrosis: the role of platelets in chronic changes induced by bleomycin
2021, Journal of Pharmacological and Toxicological MethodsCitation Excerpt :Indeed, platelets are a major source of TGF-β (Momi et al., 2017; Pitchford et al., 2019; Wilson & Wynn, 2009) and the observation of platelet accumulation into lung tissue and the correlation between platelet numbers in the BAL and fibrotic markers in this model would suggest a direct contribution of platelets to the pathological response. Platelet recruitment into lungs has also been observed in models of asthma, sterile inflammation, and bacterial infection, and it has recently been reported that platelet recruitment into the lung can be independent of the recruitment of other inflammatory cells (Eisinger et al., 2018; Lefrancais et al., 2017; Momi et al., 2017; Page, 1988; Petito et al., 2018; Pitchford et al., 2019; Zaid et al., 2020). Furthermore, we have previously reported that platelet depletion in a murine model of chronic allergic lung inflammation was able to reduce remodelling events in the airway wall, processes that could not be inhibited by the chronic administration of dexamethasone that was otherwise effective at suppressing airways inflammation (Cleary et al., 2019).
Platelets
2021, Encyclopedia of Respiratory Medicine, Second EditionPharmacological strategies for targeting platelet activation in asthma
2019, Current Opinion in PharmacologyCitation Excerpt :This contradiction would suggest that the nature of participation of platelets in inflammatory events of host defence is fundamentally different to the essential platelet activation during haemostasis [19]. A concept for a dichotomy in platelet activation was proposed by Page in 1988 [20], and an implication is that drugs developed to target platelet activation in inflammatory diseases will need to be different to current anti-platelet drugs used for secondary prevention of thrombosis. Platelets are an attractive target as a solution for novel anti-inflammatory therapies for a number of reasons: 1) the involvement of platelets in inflammation can occur at various levels of the immune response, and have substantial roles in critical processes (for example platelet-dependent leukocyte recruitment), therefore, to target platelet activation would reduce the likelihood of operational redundancy; 2) rapid anti-inflammatory effects are induced experimentally by targeting platelet activation via GPCR antagonism; 3) the short platelet lifespan (8–10 days) offers an opportunity to manipulate windows of anti-inflammatory therapy when host-defence to an opportunistic infection cannot be compromised.
A dichotomy in platelet activation: Evidence of different functional platelet responses to inflammatory versus haemostatic stimuli
2018, Thrombosis ResearchCitation Excerpt :In vivo studies have also supported the hypothesis that the pro-inflammatory role of platelets is distinct from the role of platelets in haemostasis, as platelet-dependent inflammatory cell recruitment may be inhibited by drugs not influencing platelet aggregation [9,10]. These observations, describing a divergence in platelet functions, support the hypothesis of the existence of a 'dichotomy in platelet activation' originally proposed by one of us nearly two decades ago [24], with the triggering of different platelet functions depending on the inflammatory versus haemostatic nature of the stimulus. The aim of the present study was therefore to systematically evaluate in vitro the effect of a panel of either agonists classically associated with haemostatic processes (ADP, collagen [Coll], convulxin [CVX], epinephrine [Epi], TRAP-6 and the TxA2 analogue U46619) or inflammatory stimuli (fMLP, histamine [Hist], interleukin-1β [IL-1β], lipopolysaccharide [LPS], macrophage-derived chemokine-[MDC/CCL22], stromal cell-derived factor-1α-[SDF-1α/CXCL12] and serotonin [5-HT]) on a series of primarily haemostatic or inflammatory functions of platelets.
Diverse signalling of the platelet P2Y<inf>1</inf> receptor leads to a dichotomy in platelet function
2018, European Journal of PharmacologyCitation Excerpt :We were the first to identify a divergent, or ‘biased’, signalling event centred on the platelet purinergic P2Y1 receptor that controls leukocyte recruitment during inflammation, but that does not affect haemostasis (Amison et al., 2015, 2017b). This divergence in platelet function supports the hypothesis: ‘Dichotomy in platelet activation’, whereby platelet activation is considered distinct following activation with inflammatory stimuli versus aggregatory stimuli (Page, 1988). The role of purinergic receptor activation in the regulation of leukocyte activation, adhesion molecule expression and motility has received considerable attention (Chen et al., 2006; Ferrari et al., 2016).