دورية أكاديمية
أعرض في EDS

Platelet Activation Pathways Controlling Reversible Integrin αIIbβ3 Activation.

التفاصيل البيبلوغرافية
العنوان: Platelet Activation Pathways Controlling Reversible Integrin αIIbβ3 Activation.
المؤلفون: Zou J; Platelet (patho)physiology, Synapse Research Institute, Maastricht, The Netherlands.; Department of Biochemistry and Internal Medicine, Maastricht University Medical Center + , Maastricht, The Netherlands., Sun S; Platelet (patho)physiology, Synapse Research Institute, Maastricht, The Netherlands.; Department of Biochemistry and Internal Medicine, Maastricht University Medical Center + , Maastricht, The Netherlands., De Simone I; Platelet (patho)physiology, Synapse Research Institute, Maastricht, The Netherlands., Ten Cate H; Department of Biochemistry and Internal Medicine, Maastricht University Medical Center + , Maastricht, The Netherlands., de Groot PG; Platelet (patho)physiology, Synapse Research Institute, Maastricht, The Netherlands., de Laat B; Platelet (patho)physiology, Synapse Research Institute, Maastricht, The Netherlands., Roest M; Platelet (patho)physiology, Synapse Research Institute, Maastricht, The Netherlands., Heemskerk JWM; Platelet (patho)physiology, Synapse Research Institute, Maastricht, The Netherlands., Swieringa F; Platelet (patho)physiology, Synapse Research Institute, Maastricht, The Netherlands.
المصدر: TH open : companion journal to thrombosis and haemostasis [TH Open] 2024 Jun 22; Vol. 8 (2), pp. e232-e242. Date of Electronic Publication: 2024 Jun 22 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Thieme Country of Publication: Germany NLM ID: 101715740 Publication Model: eCollection Cited Medium: Internet ISSN: 2512-9465 (Electronic) Linking ISSN: 25129465 NLM ISO Abbreviation: TH Open Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Stuttgart : Thieme, [2017]-
مستخلص: Background  Agonist-induced platelet activation, with the integrin αIIbβ3 conformational change, is required for fibrinogen binding. This is considered reversible under specific conditions, allowing a second phase of platelet aggregation. The signaling pathways that differentiate between a permanent or transient activation state of platelets are poorly elucidated. Objective  To explore platelet signaling mechanisms induced by the collagen receptor glycoprotein VI (GPVI) or by protease-activated receptors (PAR) for thrombin that regulate time-dependent αIIbβ3 activation. Methods  Platelets were activated with collagen-related peptide (CRP, stimulating GPVI), thrombin receptor-activating peptides, or thrombin (stimulating PAR1 and/or 4). Integrin αIIbβ3 activation and P-selectin expression was assessed by two-color flow cytometry. Signaling pathway inhibitors were applied before or after agonist addition. Reversibility of platelet spreading was studied by microscopy. Results  Platelet pretreatment with pharmacological inhibitors decreased GPVI- and PAR-induced integrin αIIbβ3 activation and P-selectin expression in the target order of protein kinase C (PKC) > glycogen synthase kinase 3 > β-arrestin > phosphatidylinositol-3-kinase. Posttreatment revealed secondary αIIbβ3 inactivation (not P-selectin expression), in the same order, but this reversibility was confined to CRP and PAR1 agonist. Combined inhibition of conventional and novel PKC isoforms was most effective for integrin closure. Pre- and posttreatment with ticagrelor, blocking the P2Y 12 adenosine diphosphate (ADP) receptor, enhanced αIIbβ3 inactivation. Spreading assays showed that PKC or P2Y 12 inhibition provoked a partial conversion from filopodia to a more discoid platelet shape. Conclusion  PKC and autocrine ADP signaling contribute to persistent integrin αIIbβ3 activation in the order of PAR1/GPVI > PAR4 stimulation and hence to stabilized platelet aggregation. These findings are relevant for optimization of effective antiplatelet treatment.
Competing Interests: Conflict of Interest None declared.
(The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. ( https://creativecommons.org/licenses/by/4.0/ ).)
References: Thromb Res. 2017 Nov;159:100-108. (PMID: 29078099)
Int J Mol Sci. 2021 Sep 30;22(19):. (PMID: 34638997)
Biochem J. 1989 Oct 15;263(2):377-85. (PMID: 2574568)
Blood. 2012 Apr 26;119(17):4056-65. (PMID: 22371881)
FEBS Lett. 2001 Sep 14;505(2):281-90. (PMID: 11566191)
J Biol Chem. 2009 Dec 4;284(49):33750-62. (PMID: 19815551)
Blood. 1999 Dec 15;94(12):4156-65. (PMID: 10590060)
Nat Rev Cardiol. 2019 Mar;16(3):166-179. (PMID: 30429532)
J Thromb Haemost. 2020 Jan;18(1):6-16. (PMID: 31549766)
Int J Mol Sci. 2021 Dec 29;23(1):. (PMID: 35008781)
Int J Mol Sci. 2022 Oct 19;23(20):. (PMID: 36293367)
Int J Mol Sci. 2022 Jan 01;23(1):. (PMID: 35008919)
Nat Biotechnol. 2011 Oct 30;29(11):1039-45. (PMID: 22037377)
FEBS Lett. 2011 Jun 23;585(12):1711-6. (PMID: 21596041)
Blood. 2016 Nov 24;128(21):2538-2549. (PMID: 27625359)
Haematologica. 2015 Sep;100(9):1131-8. (PMID: 26113418)
Physiol Rev. 2013 Jan;93(1):327-58. (PMID: 23303912)
Biochem J. 2002 Dec 1;368(Pt 2):535-43. (PMID: 12215172)
Trends Pharmacol Sci. 2021 Apr;42(4):283-299. (PMID: 33581873)
J Biol Chem. 2013 May 10;288(19):13325-36. (PMID: 23519467)
J Clin Invest. 2009 Feb;119(2):399-407. (PMID: 19147982)
Arterioscler Thromb Vasc Biol. 2009 May;29(5):699-705. (PMID: 19213940)
Arterioscler Thromb Vasc Biol. 2020 Sep;40(9):2127-2142. (PMID: 32698684)
J Hematol Oncol. 2019 Mar 7;12(1):26. (PMID: 30845955)
Eur J Pharmacol. 2018 Oct 15;837:45-52. (PMID: 30170065)
J Biol Chem. 2004 Mar 12;279(11):10020-31. (PMID: 14699102)
ACS Med Chem Lett. 2013 Jul 20;4(9):846-851. (PMID: 24611085)
Cell Calcium. 2023 Jun;112:102738. (PMID: 37060673)
Biochem J. 1991 Jan 1;273(Pt 1):115-20. (PMID: 1846526)
Spectrochim Acta A Mol Biomol Spectrosc. 2019 Feb 15;209:150-164. (PMID: 30388586)
J Biol Chem. 2010 Jul 23;285(30):23410-9. (PMID: 20479008)
Thromb Haemost. 2022 May;122(5):726-738. (PMID: 34689320)
PLoS One. 2010 Apr 12;5(4):e10130. (PMID: 20405028)
ACS Chem Biol. 2016 Jul 15;11(7):1880-90. (PMID: 27119457)
J Thromb Haemost. 2023 May;21(5):1289-1306. (PMID: 36754678)
Blood. 2016 Dec 8;128(23):2717-2728. (PMID: 27694321)
Res Pract Thromb Haemost. 2019 Jul 16;3(4):615-625. (PMID: 31624781)
Blood. 2009 Oct 1;114(14):3056-63. (PMID: 19587372)
Nat Commun. 2023 Jun 7;14(1):3328. (PMID: 37286565)
PLoS One. 2021 Mar 3;16(3):e0247425. (PMID: 33657162)
Platelets. 2021 Oct 3;32(7):863-871. (PMID: 33356720)
Br J Pharmacol. 2010 Oct;161(3):643-58. (PMID: 20880402)
Blood. 2013 Mar 7;121(10):1850-7. (PMID: 23303820)
فهرسة مساهمة: Keywords: P-selectin; glycoprotein VI; integrin αIIbβ3; protease-activated receptors; protein kinase C
تواريخ الأحداث: Date Created: 20240624 Latest Revision: 20240625
رمز التحديث: 20240625
مُعرف محوري في PubMed: PMC11193594
DOI: 10.1055/s-0044-1786987
PMID: 38911141
قاعدة البيانات: MEDLINE
الوصف
تدمد:2512-9465
DOI:10.1055/s-0044-1786987