Platelet-derived microparticles stimulated by anti-β2GPI/β2GPI complexes induce pyroptosis of endothelial cells in antiphospholipid syndrome
Platelet microparticles (PMPs) are vesicles that are released by platelets into the extracellular space and play a role in antiphospholipid antibody syndromes. PMPs have recently been recognized as a new and viable cell. There is growing evidence that the anti-β2 glycoprotein (GPI)/β2GPI complex is...
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Format: | Article |
Language: | English |
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Taylor & Francis Group
2023-12-01
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Series: | Platelets |
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Online Access: | http://dx.doi.org/10.1080/09537104.2022.2156492 |
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author | Longjiang Di Caijun Zha Yanhong Liu |
author_facet | Longjiang Di Caijun Zha Yanhong Liu |
author_sort | Longjiang Di |
collection | DOAJ |
description | Platelet microparticles (PMPs) are vesicles that are released by platelets into the extracellular space and play a role in antiphospholipid antibody syndromes. PMPs have recently been recognized as a new and viable cell. There is growing evidence that the anti-β2 glycoprotein (GPI)/β2GPI complex is associated with aberrant activation of PMPs. Although studies suggest that aberrant activation of PMPs may lead to inflammatory necrosis of endothelial cells, the underlying mechanisms remain unclear. We found that although the difference in the number of PMPs was not statistically significant, NLR family pyrin domain containing 3 (NLRP3) within PMPs was increased during stimulation of anti-β2GPI/β2GPI complexes. Furthermore, we demonstrated that anti-β2GPI/β2GPI complex-induced PMPs effectively stimulated endothelial cell pyroptosis via the NLRP3/nuclear factor (NF)-κB/gasdermin D (GSDMD) signaling pathway as well as the NLRP3/Caspase-1 signaling pathway. Additionally, inhibition of NLRP3 expression in PMPs effectively reduced the inflammatory response and pyroptosis in endothelial cells. Our data suggest that PMPs aberrantly activated by anti-β2GPI/β2GPI complexes play a vital role in endothelial cell pyroptosis, and these studies provide major insights into the mechanisms of thrombosis during the treatment of antiphospholipid antibody syndrome. |
first_indexed | 2024-03-12T00:25:11Z |
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id | doaj.art-7095b95f03604ad3b6d9388fa0247bcc |
institution | Directory Open Access Journal |
issn | 0953-7104 1369-1635 |
language | English |
last_indexed | 2024-03-12T00:25:11Z |
publishDate | 2023-12-01 |
publisher | Taylor & Francis Group |
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series | Platelets |
spelling | doaj.art-7095b95f03604ad3b6d9388fa0247bcc2023-09-15T10:38:11ZengTaylor & Francis GroupPlatelets0953-71041369-16352023-12-0134110.1080/09537104.2022.21564922156492Platelet-derived microparticles stimulated by anti-β2GPI/β2GPI complexes induce pyroptosis of endothelial cells in antiphospholipid syndromeLongjiang Di0Caijun Zha1Yanhong Liu2Second Affiliated Hospital of Harbin Medical UniversitySecond Affiliated Hospital of Harbin Medical UniversitySecond Affiliated Hospital of Harbin Medical UniversityPlatelet microparticles (PMPs) are vesicles that are released by platelets into the extracellular space and play a role in antiphospholipid antibody syndromes. PMPs have recently been recognized as a new and viable cell. There is growing evidence that the anti-β2 glycoprotein (GPI)/β2GPI complex is associated with aberrant activation of PMPs. Although studies suggest that aberrant activation of PMPs may lead to inflammatory necrosis of endothelial cells, the underlying mechanisms remain unclear. We found that although the difference in the number of PMPs was not statistically significant, NLR family pyrin domain containing 3 (NLRP3) within PMPs was increased during stimulation of anti-β2GPI/β2GPI complexes. Furthermore, we demonstrated that anti-β2GPI/β2GPI complex-induced PMPs effectively stimulated endothelial cell pyroptosis via the NLRP3/nuclear factor (NF)-κB/gasdermin D (GSDMD) signaling pathway as well as the NLRP3/Caspase-1 signaling pathway. Additionally, inhibition of NLRP3 expression in PMPs effectively reduced the inflammatory response and pyroptosis in endothelial cells. Our data suggest that PMPs aberrantly activated by anti-β2GPI/β2GPI complexes play a vital role in endothelial cell pyroptosis, and these studies provide major insights into the mechanisms of thrombosis during the treatment of antiphospholipid antibody syndrome.http://dx.doi.org/10.1080/09537104.2022.2156492antiphospholipid antibody syndromeplatelet-derived microparticlespyroptosis |
spellingShingle | Longjiang Di Caijun Zha Yanhong Liu Platelet-derived microparticles stimulated by anti-β2GPI/β2GPI complexes induce pyroptosis of endothelial cells in antiphospholipid syndrome Platelets antiphospholipid antibody syndrome platelet-derived microparticles pyroptosis |
title | Platelet-derived microparticles stimulated by anti-β2GPI/β2GPI complexes induce pyroptosis of endothelial cells in antiphospholipid syndrome |
title_full | Platelet-derived microparticles stimulated by anti-β2GPI/β2GPI complexes induce pyroptosis of endothelial cells in antiphospholipid syndrome |
title_fullStr | Platelet-derived microparticles stimulated by anti-β2GPI/β2GPI complexes induce pyroptosis of endothelial cells in antiphospholipid syndrome |
title_full_unstemmed | Platelet-derived microparticles stimulated by anti-β2GPI/β2GPI complexes induce pyroptosis of endothelial cells in antiphospholipid syndrome |
title_short | Platelet-derived microparticles stimulated by anti-β2GPI/β2GPI complexes induce pyroptosis of endothelial cells in antiphospholipid syndrome |
title_sort | platelet derived microparticles stimulated by anti β2gpi β2gpi complexes induce pyroptosis of endothelial cells in antiphospholipid syndrome |
topic | antiphospholipid antibody syndrome platelet-derived microparticles pyroptosis |
url | http://dx.doi.org/10.1080/09537104.2022.2156492 |
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