The inhibition of oxygen radical release from human neutrophils by resting platelets is reversed by administration of acetylsalicylic acid or clopidogrel

Reinisch, Carol L.; Dunzendorfer, Stefan; Pechlaner, Christoph; Ricevuti, Giovanni; Wiedermann, Christian J.

doi:10.1080/10715760100300401

Cited by 16 publications

(17 citation statements)

References 12 publications

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“…Others have shown that platelets can limit neutrophil function in response to non-TLR agonists. Platelets have been shown to reduce elastase secretion 25 and reduce production of reactive oxygen species (ROS) 26,27 by neutrophils stimulated with the calcium ionophore, A23187, or the chemotactic protein, fMLP.…”

Section: Discussionmentioning

confidence: 99%

Platelets regulate leucocyte responses to Toll‐like receptor stimulation

et al. 2018

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ObjectivesPlatelets are important regulators of vascular thrombosis and inflammation and are known to express Toll‐like receptors (TLRs). Through TLRs, platelets mediate a number of responses by interacting with leucocytes. Here, we report the extent to which platelets modulate in vitro peripheral blood mononuclear cells (PBMCs) and granulocyte responses to TLR4, TLR2/1 and TLR2/6 stimulation in healthy subjects.MethodsPeripheral blood mononuclear cells and granulocytes from 10 healthy volunteers were cultured alone or cocultured with platelets. Cultures were left unstimulated or stimulated with 1 or 100 ng mL−1 of either LPS (TLR4 agonist), Pam3CSK4 (TLR2/1 agonist) or fibroblast‐stimulating lipopeptide (FSL)‐1 (TLR2/6 agonist). Neutrophil activation (CD66b expression), monocyte activation (HLA‐DR), granulocyte elastase production and PBMC cytokine and chemokine production were examined.ResultsPlatelet coculture decreased neutrophil CD66b expression in response to LPS, Pam3CSK4 and FSL‐1, and modestly decreased monocyte HLA‐DR expression in response to low‐dose LPS. Platelets reduced granulocyte elastase secretion in response to low doses of all TLR agonists tested. In response to LPS, platelet coculture reduced IL‐6, tumor necrosis factor (TNF)‐α and MIP‐1β production, and increased IL‐10 production by PBMCs. In response to FSL‐1, platelets increased IL‐6, IL‐10 and MIP‐1β production, but reduced TNF‐α production. Platelet coculture did not alter PBMC cytokine/chemokine production in response to Pam3CSK4.ConclusionThis study challenges the notion that platelets act solely in a pro‐inflammatory manner. Rather, platelets are complex immunomodulators that regulate leucocyte responses to TLR stimulation in a TLR agonist‐specific manner. Platelets may modulate leucocyte responses to dampen inflammation, and this platelet effect may play an important role in reducing inflammation‐mediated host damage.

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Section: Discussionmentioning

confidence: 99%

Platelets regulate leucocyte responses to Toll‐like receptor stimulation

et al. 2018

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“…The method for analyzing the relationship between the antiplatelet and antioxidant activities of hindered phenols was carried out by the probabilistic histogram method (Mandel 1988). For this, all the studied substances were divided into classes with different levels of activity.…”

Section: Methodsmentioning

confidence: 99%

“…Considering that oxidative stress is caused by the interaction of platelets and blood vessels (Sies 2015, Fuentes et al 2019, it is of importance to search for and develop combination antiplatelet and antioxidant drugs (Reinisch et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Antiplatelet activity of new derivatives of benzimidazole containing sterically hindered phenolic group in their structure

Spasov¹,

Kucheryavenko²,

Gaidukova³

et al. 2020

RRP

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Citation: Spasov AA, Kucheryavenko AF, Gaidukova KA, Kosolapov VA, Zhukovskaya ON (2020) Antiplatelet activity of new derivatives of benzimidazole containing sterically hindered phenolic group in their structure. Research Results in Pharmacology 6(1): 1-9. https://doi. AbstractIntroduction: Cardiovascular diseases are currently the leading cause of global disability and mortality. According to the centers for disease control and prevention, the average life expectancy of a person would be 10 years longer but for a high prevalence of cardiovascular diseases, and if antiplatelet drugs and special therapy were used. Materials and methods:Antiplatelet activity of the novel benzimidazole derivatives containing a sterically hindered phenolic group in their structure has been investigated in vitro, using a model of ADP-induced platelet aggregation of rabbit's plasma. The compounds exhibiting high antiplatelet activity and acetylsalicylic acid, as a reference drug, were examined for antioxidant properties in an ascorbate-dependent model of lipid peroxidation.Results: It was established that the compounds with high antiplatelet activity demonstrated the pronounced antioxidant action. The compound RU-1144 (1-(3,5-ditretbutyl-4-hydroxyphenyl) -1-hydroxypropyl)-phenyl-pyrimidobenzimidazole hydrochloride), in in vitro experiments, had a pronounced antiplatelet activity, surpassing the reference drug acetylsalicylic acid by 21.8 times; in the study of antioxidant activity, the leader compound was inferior to the reference drug dibunol by 1.7 times. By inhibiting intravascular platelet aggregation in vivo, this compound exceeded acetylsalicylic acid by 1.5 times and was slightly inferior to clopidogrel by 1.4 times. Discussion:Benzimidazole derivatives with a hindered phenolic substituent in their structure exhibited antiplatelet and antioxidant properties. It was established that the compounds with high antiplatelet activity demonstrated the pronounced antioxidant action. Conclusion:The chemical class of benzimidazole derivatives with a hindered phenolic substituent in their structure is promising for the search for new antiaggregant and antioxidant drugs.

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“…Both activation and suppression of neutrophilic functions by the action of platelets have been reported. We found that products released from platelets activate leukocytic phagocytosis .…”

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confidence: 99%

An immunohistochemical study of human platelets using a rabbit antibody against H18‐K24 of apolipoprotein CIII (HATKTAK)

Yamanaka

Sakamoto

Nakagawa

et al. 2013

Pathology International

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H18-K24 of human apolipopotein CIII (Apo CIII) (HATKTAK) is an activator of the macromolecular activators of phagocytosis from platelets (MAPPs). Using a rabbit antibody against HATKTAK, we performed an immunohistochemical study of human platelets. Indirect ELISA showed that this antibody reacts with Apo CIII-derived peptides with a C-terminal of HATKTAK, but not with Apo CIII. Immunoelectron microscopy revealed that reaction of anti-HATKTAK antibody occurred in the pseudopods of activated platelets. In blood coagula produced from the peripheral blood and formalin-fixed after various incubation periods, reaction of this antibody with platelets appeared rapidly with a peak at 3 to 6 h of incubation, and then diminished gradually. Leukocytes in the blood coagula were stained strongly positive. In tissue sections, fresh thrombi and hemorrhages with slight fibrin formation revealed a positive response of platelets to anti-HATKTAK antibody, whereas older ones with leukocytic infiltration, fibrin formation and organization did not. In addition to platelets, endothelial cells and leukocytes were stained positive by anti-HATKTAK antibody. All of the positive reactions by anti-HATKTAK antibody disappeared or diminished by co-incubation with HATKTAK. In conclusion, the anti-HATKTAK antibody reveals platelets during the early phase of activation.

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The inhibition of oxygen radical release from human neutrophils by resting platelets is reversed by administration of acetylsalicylic acid or clopidogrel

Cited by 16 publications

References 12 publications

Platelets regulate leucocyte responses to Toll‐like receptor stimulation

Platelets regulate leucocyte responses to Toll‐like receptor stimulation

Antiplatelet activity of new derivatives of benzimidazole containing sterically hindered phenolic group in their structure

An immunohistochemical study of human platelets using a rabbit antibody against H18‐K24 of apolipoprotein CIII (HATKTAK)

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