PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity.
Hypertension is known to be associated with platelet overactivity, but the direct effects of hydrostatic pressure on platelet function remain unclear. The present study sought to investigate whether elevated hydrostatic pressure is responsible for platelet activation and to address the potential rol...
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| Format: | Article |
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Public Library of Science (PLoS)
2014-01-01
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| Series: | PLoS ONE |
| Online Access: | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089654&type=printable |
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| author | Fang Rao Ren-Qiang Yang Xiao-Shu Chen Jin-Song Xu Hui-Min Fu Hai Su Ling Wang |
| author_facet | Fang Rao Ren-Qiang Yang Xiao-Shu Chen Jin-Song Xu Hui-Min Fu Hai Su Ling Wang |
| author_sort | Fang Rao |
| collection | DOAJ |
| description | Hypertension is known to be associated with platelet overactivity, but the direct effects of hydrostatic pressure on platelet function remain unclear. The present study sought to investigate whether elevated hydrostatic pressure is responsible for platelet activation and to address the potential role of peroxisome proliferator-activated receptor-γ (PPARγ). We observed that hypertensive patients had significantly higher platelet volume and rate of ADP-induced platelets aggregation compared to the controls. In vitro, Primary human platelets were cultured under standard (0 mmHg) or increased (120, 180, 240 mmHg) hydrostatic pressure for 18 h. Exposure to elevated pressure was associated with morphological changes in platelets. Platelet aggregation and PAC-1 (the active confirmation of GPIIb/IIIa) binding were increased, CD40L was translocated from cytoplasm to the surface of platelet and soluble CD40L (sCD40L) was released into the medium in response to elevated hydrostatic pressure (180 and 240 mmHg). The PPARγ activity was up-regulated as the pressure was increased from 120 mmHg to 180 mmHg. Pressure-induced platelet aggregation, PAC-1 binding, and translocation and release of CD40L were all attenuated by the PPARγ agonist Thiazolidinediones (TZDs). These results demonstrate that platelet activation and aggregation are increased by exposure to elevated pressure and that PPARγ may modulate platelet activation induced by high hydrostatic pressure. |
| format | Article |
| id | doaj-art-174b00a7068640a9ab0003bc8761bfa6 |
| institution | DOAJ |
| issn | 1932-6203 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj-art-174b00a7068640a9ab0003bc8761bfa62025-08-20T03:11:54ZengPublic Library of Science (PLoS)PLoS ONE1932-62032014-01-0192e8965410.1371/journal.pone.0089654PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity.Fang RaoRen-Qiang YangXiao-Shu ChenJin-Song XuHui-Min FuHai SuLing WangHypertension is known to be associated with platelet overactivity, but the direct effects of hydrostatic pressure on platelet function remain unclear. The present study sought to investigate whether elevated hydrostatic pressure is responsible for platelet activation and to address the potential role of peroxisome proliferator-activated receptor-γ (PPARγ). We observed that hypertensive patients had significantly higher platelet volume and rate of ADP-induced platelets aggregation compared to the controls. In vitro, Primary human platelets were cultured under standard (0 mmHg) or increased (120, 180, 240 mmHg) hydrostatic pressure for 18 h. Exposure to elevated pressure was associated with morphological changes in platelets. Platelet aggregation and PAC-1 (the active confirmation of GPIIb/IIIa) binding were increased, CD40L was translocated from cytoplasm to the surface of platelet and soluble CD40L (sCD40L) was released into the medium in response to elevated hydrostatic pressure (180 and 240 mmHg). The PPARγ activity was up-regulated as the pressure was increased from 120 mmHg to 180 mmHg. Pressure-induced platelet aggregation, PAC-1 binding, and translocation and release of CD40L were all attenuated by the PPARγ agonist Thiazolidinediones (TZDs). These results demonstrate that platelet activation and aggregation are increased by exposure to elevated pressure and that PPARγ may modulate platelet activation induced by high hydrostatic pressure.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089654&type=printable |
| spellingShingle | Fang Rao Ren-Qiang Yang Xiao-Shu Chen Jin-Song Xu Hui-Min Fu Hai Su Ling Wang PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity. PLoS ONE |
| title | PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity. |
| title_full | PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity. |
| title_fullStr | PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity. |
| title_full_unstemmed | PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity. |
| title_short | PPARγ ligands decrease hydrostatic pressure-induced platelet aggregation and proinflammatory activity. |
| title_sort | pparγ ligands decrease hydrostatic pressure induced platelet aggregation and proinflammatory activity |
| url | https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0089654&type=printable |
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