Increased prostacyclin levels inhibit the aggregation and activation of platelets via the PI3K-AKT pathway in prolonged isolated thrombocytopenia after allogeneic hematopoietic stem cell transplantation

Xiao Hui Zhang; Shi Yuan Zhou; Ru Feng; Ya Zhe Wang; Yuan Kong; Yi Zhou; Jia Min Zhang; Min Wang; Jing Zhong Zhao; Qian Ming Wang; Fei Er Feng; Xiao Lu Zhu; Feng Rong Wang; Jing Zhi Wang; Wei Han; Huan Chen; Lan Ping Xu; Yan Rong Liu; Kai Yan Liu; Xiao Jun Huang

doi:10.1016/j.thromres.2016.01.003

Increased prostacyclin levels inhibit the aggregation and activation of platelets via the PI3K-AKT pathway in prolonged isolated thrombocytopenia after allogeneic hematopoietic stem cell transplantation

Xiao Hui Zhang^*, Shi Yuan Zhou, Ru Feng, Ya Zhe Wang, Yuan Kong, Yi Zhou, Jia Min Zhang, Min Wang, Jing Zhong Zhao, Qian Ming Wang, Fei Er Feng, Xiao Lu Zhu, Feng Rong Wang, Jing Zhi Wang, Wei Han, Huan Chen, Lan Ping Xu, Yan Rong Liu, Kai Yan Liu, Xiao Jun Huang

^*Corresponding author for this work

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8 Citations (Scopus)

Abstract

Objectives The aim of this study was to investigate the role of prostacyclin (PGI₂) in prolonged isolated thrombocytopenia (PT) following allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the effect of PGI₂ on the activation and aggregation of platelets in PT. Methods We enrolled 37 patients with PT and 36 controls following allo-HSCT in this study. Platelet aggregation and activation and PGI₂ levels were measured. Endothelial progenitor cells (EPCs) from either PT or control patients were cultured ex vivo with serum from either PT or control patients. PGI₂ secretions were then measured. PGI₂ was added to the platelets ex vivo, and platelet aggregation and activation and PI3K/Akt phosphorylation were analyzed. Results A higher PGI₂ level was observed in the PT patients. The activation and aggregation of platelets were significantly lower in the PT patients. EPCs from PT patients cultured in PT serum secreted higher levels of PGI₂, and PGI₂ inhibited platelet activation and aggregation in a concentration-dependent manner ex vivo. PI3K/Akt phosphorylation of platelets was regulated by PGI₂ after allo-HSCT. Disease status, serum PGI₂ level and platelet aggregation were independent risk factors in patients with PT after allo-HSCT. Conclusions Higher PGI₂ levels and lower platelet activation and aggregation occurred simultaneously in PT patients. PGI₂ inhibited platelet activation and aggregation, probably by regulating the phosphorylation of PI3K/Akt.

Original language	English
Pages (from-to)	1-9
Number of pages	9
Journal	Thrombosis Research
Volume	139
DOIs	https://doi.org/10.1016/j.thromres.2016.01.003
Publication status	Published - 1 Mar 2016
Externally published	Yes

Keywords

Hematopoietic stem cell transplantation
Platelet activation
Platelet aggregation
Prolonged isolated thrombocytopenia
Prostacyclin

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10.1016/j.thromres.2016.01.003

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Zhang, X. H., Zhou, S. Y., Feng, R., Wang, Y. Z., Kong, Y., Zhou, Y., Zhang, J. M., Wang, M., Zhao, J. Z., Wang, Q. M., Feng, F. E., Zhu, X. L., Wang, F. R., Wang, J. Z., Han, W., Chen, H., Xu, L. P., Liu, Y. R., Liu, K. Y., & Huang, X. J. (2016). Increased prostacyclin levels inhibit the aggregation and activation of platelets via the PI3K-AKT pathway in prolonged isolated thrombocytopenia after allogeneic hematopoietic stem cell transplantation. Thrombosis Research, 139, 1-9. https://doi.org/10.1016/j.thromres.2016.01.003

@article{b72737e04efa4ea284b13620752837da,

title = "Increased prostacyclin levels inhibit the aggregation and activation of platelets via the PI3K-AKT pathway in prolonged isolated thrombocytopenia after allogeneic hematopoietic stem cell transplantation",

abstract = "Objectives The aim of this study was to investigate the role of prostacyclin (PGI2) in prolonged isolated thrombocytopenia (PT) following allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the effect of PGI2 on the activation and aggregation of platelets in PT. Methods We enrolled 37 patients with PT and 36 controls following allo-HSCT in this study. Platelet aggregation and activation and PGI2 levels were measured. Endothelial progenitor cells (EPCs) from either PT or control patients were cultured ex vivo with serum from either PT or control patients. PGI2 secretions were then measured. PGI2 was added to the platelets ex vivo, and platelet aggregation and activation and PI3K/Akt phosphorylation were analyzed. Results A higher PGI2 level was observed in the PT patients. The activation and aggregation of platelets were significantly lower in the PT patients. EPCs from PT patients cultured in PT serum secreted higher levels of PGI2, and PGI2 inhibited platelet activation and aggregation in a concentration-dependent manner ex vivo. PI3K/Akt phosphorylation of platelets was regulated by PGI2 after allo-HSCT. Disease status, serum PGI2 level and platelet aggregation were independent risk factors in patients with PT after allo-HSCT. Conclusions Higher PGI2 levels and lower platelet activation and aggregation occurred simultaneously in PT patients. PGI2 inhibited platelet activation and aggregation, probably by regulating the phosphorylation of PI3K/Akt.",

keywords = "Hematopoietic stem cell transplantation, Platelet activation, Platelet aggregation, Prolonged isolated thrombocytopenia, Prostacyclin",

author = "Zhang, {Xiao Hui} and Zhou, {Shi Yuan} and Ru Feng and Wang, {Ya Zhe} and Yuan Kong and Yi Zhou and Zhang, {Jia Min} and Min Wang and Zhao, {Jing Zhong} and Wang, {Qian Ming} and Feng, {Fei Er} and Zhu, {Xiao Lu} and Wang, {Feng Rong} and Wang, {Jing Zhi} and Wei Han and Huan Chen and Xu, {Lan Ping} and Liu, {Yan Rong} and Liu, {Kai Yan} and Huang, {Xiao Jun}",

year = "2016",

month = mar,

day = "1",

doi = "10.1016/j.thromres.2016.01.003",

language = "English",

volume = "139",

pages = "1--9",

journal = "Thrombosis Research",

issn = "0049-3848",

publisher = "Elsevier Ltd.",

}

Zhang, XH, Zhou, SY, Feng, R, Wang, YZ, Kong, Y, Zhou, Y, Zhang, JM, Wang, M, Zhao, JZ, Wang, QM, Feng, FE, Zhu, XL, Wang, FR, Wang, JZ, Han, W, Chen, H, Xu, LP, Liu, YR, Liu, KY & Huang, XJ 2016, 'Increased prostacyclin levels inhibit the aggregation and activation of platelets via the PI3K-AKT pathway in prolonged isolated thrombocytopenia after allogeneic hematopoietic stem cell transplantation', Thrombosis Research, vol. 139, pp. 1-9. https://doi.org/10.1016/j.thromres.2016.01.003

Increased prostacyclin levels inhibit the aggregation and activation of platelets via the PI3K-AKT pathway in prolonged isolated thrombocytopenia after allogeneic hematopoietic stem cell transplantation. / Zhang, Xiao Hui; Zhou, Shi Yuan; Feng, Ru et al.
In: Thrombosis Research, Vol. 139, 01.03.2016, p. 1-9.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Increased prostacyclin levels inhibit the aggregation and activation of platelets via the PI3K-AKT pathway in prolonged isolated thrombocytopenia after allogeneic hematopoietic stem cell transplantation

AU - Zhang, Xiao Hui

AU - Zhou, Shi Yuan

AU - Feng, Ru

AU - Wang, Ya Zhe

AU - Kong, Yuan

AU - Zhou, Yi

AU - Zhang, Jia Min

AU - Wang, Min

AU - Zhao, Jing Zhong

AU - Wang, Qian Ming

AU - Feng, Fei Er

AU - Zhu, Xiao Lu

AU - Wang, Feng Rong

AU - Wang, Jing Zhi

AU - Han, Wei

AU - Chen, Huan

AU - Xu, Lan Ping

AU - Liu, Yan Rong

AU - Liu, Kai Yan

AU - Huang, Xiao Jun

PY - 2016/3/1

Y1 - 2016/3/1

N2 - Objectives The aim of this study was to investigate the role of prostacyclin (PGI2) in prolonged isolated thrombocytopenia (PT) following allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the effect of PGI2 on the activation and aggregation of platelets in PT. Methods We enrolled 37 patients with PT and 36 controls following allo-HSCT in this study. Platelet aggregation and activation and PGI2 levels were measured. Endothelial progenitor cells (EPCs) from either PT or control patients were cultured ex vivo with serum from either PT or control patients. PGI2 secretions were then measured. PGI2 was added to the platelets ex vivo, and platelet aggregation and activation and PI3K/Akt phosphorylation were analyzed. Results A higher PGI2 level was observed in the PT patients. The activation and aggregation of platelets were significantly lower in the PT patients. EPCs from PT patients cultured in PT serum secreted higher levels of PGI2, and PGI2 inhibited platelet activation and aggregation in a concentration-dependent manner ex vivo. PI3K/Akt phosphorylation of platelets was regulated by PGI2 after allo-HSCT. Disease status, serum PGI2 level and platelet aggregation were independent risk factors in patients with PT after allo-HSCT. Conclusions Higher PGI2 levels and lower platelet activation and aggregation occurred simultaneously in PT patients. PGI2 inhibited platelet activation and aggregation, probably by regulating the phosphorylation of PI3K/Akt.

AB - Objectives The aim of this study was to investigate the role of prostacyclin (PGI2) in prolonged isolated thrombocytopenia (PT) following allogeneic hematopoietic stem cell transplantation (allo-HSCT) and the effect of PGI2 on the activation and aggregation of platelets in PT. Methods We enrolled 37 patients with PT and 36 controls following allo-HSCT in this study. Platelet aggregation and activation and PGI2 levels were measured. Endothelial progenitor cells (EPCs) from either PT or control patients were cultured ex vivo with serum from either PT or control patients. PGI2 secretions were then measured. PGI2 was added to the platelets ex vivo, and platelet aggregation and activation and PI3K/Akt phosphorylation were analyzed. Results A higher PGI2 level was observed in the PT patients. The activation and aggregation of platelets were significantly lower in the PT patients. EPCs from PT patients cultured in PT serum secreted higher levels of PGI2, and PGI2 inhibited platelet activation and aggregation in a concentration-dependent manner ex vivo. PI3K/Akt phosphorylation of platelets was regulated by PGI2 after allo-HSCT. Disease status, serum PGI2 level and platelet aggregation were independent risk factors in patients with PT after allo-HSCT. Conclusions Higher PGI2 levels and lower platelet activation and aggregation occurred simultaneously in PT patients. PGI2 inhibited platelet activation and aggregation, probably by regulating the phosphorylation of PI3K/Akt.

KW - Hematopoietic stem cell transplantation

KW - Platelet activation

KW - Platelet aggregation

KW - Prolonged isolated thrombocytopenia

KW - Prostacyclin

UR - http://www.scopus.com/inward/record.url?scp=84960109137&partnerID=8YFLogxK

U2 - 10.1016/j.thromres.2016.01.003

DO - 10.1016/j.thromres.2016.01.003

M3 - Article

C2 - 26916289

AN - SCOPUS:84960109137

SN - 0049-3848

VL - 139

SP - 1

EP - 9

JO - Thrombosis Research

JF - Thrombosis Research

ER -

Increased prostacyclin levels inhibit the aggregation and activation of platelets via the PI3K-AKT pathway in prolonged isolated thrombocytopenia after allogeneic hematopoietic stem cell transplantation

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