Guang-Qiang Yao

Huazhong University of Science and Technology

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Xingwen Da

State Key Laboratory of Oncogene and Related Genes

Ao‐Di He

Huazhong University of Science and Technology

Jizhou Xiang

Huazhong University of Science and Technology

Minglu Liang

Union Hospital

Zhangyin Ming

Huazhong University of Science and Technology

Gang Liu

Guiyang Medical University

Wen Xie

Huazhong University of Science and Technology

Cunji Gao

Guangxi Normal University

Dao-Chun Wang

Wuhan University

Wenlian Xie

Huazhong University of Science and Technology

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Huazhong University of Science and Technology

Peking University

Union Hospital

Tongji Hospital

Chinese Academy of Medical Sciences & Peking Union Medical College

Wuhan University

Ministry of Education of the People's Republic of China

Soochow University

Sun Yat-sen University

Versiti Blood Center of Wisconsin

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Pentamethylquercetin (PMQ) reduces thrombus formation by inhibiting platelet function

Scientific Reports (2015)

Minglu Liang Xingwen Da Ao‐Di He Guang-Qiang Yao Wen Xie

Flavonoids exert both anti-oxidant and anti-platelet activities in vitro and in vivo. Pentamethylquercetin (PMQ), a polymethoxylated flavone derivative, has been screened for anti-carcinogenic and cardioprotective effects. However, it is unclear whether PMQ has anti-thrombotic effects. In the present study, PMQ (20 mg/kg) significantly inhibited thrombus formation in the collagen- epinephrine- induced acute pulmonary thrombosis mouse model and the ferric chloride-induced carotid injury model. To explore the mechanism, we evaluated the effects of PMQ on platelet function. We found that PMQ inhibited platelet aggregation and granule secretion induced by low dose agonists, including ADP, collagen, thrombin and U46619. Biochemical analysis revealed that PMQ inhibited collagen-, thrombin- and U46619-induced activation of Syk, PLCγ2, Akt, GSK3β and Erk1/2. Therefore, we provide the first report to show that PMQ possesses anti-thrombotic activity in vivo and inhibited platelet function in vitro, suggesting that PMQ may represent a potential therapeutic candidate for the prevention or treatment of thrombotic disorders.

10.1038/srep11142

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The Role of FcγRIIa and TGF-β1/KLF6 Pathway in Platelet's Promoting Hepatocellular Carcinoma Cells Growth

Blood (2014)

Ao‐Di He Minglu Liang Gang Liu Xingwen Da Guang-Qiang Yao

10.1182/blood.v124.21.1429.1429

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Platelet releasates promote the proliferation of hepatocellular carcinoma cells by suppressing the expression of KLF6

Scientific Reports (2017)

Ao‐Di He Wen Xie Wei Song Yuanyuan Ma Gang Liu

Platelets in the primary tumor microenvironment play crucial roles in the regulation of tumor progression, but the mechanisms underlying are poorly understood. Here, we report that platelet releasates exerted a proliferative effect on hepatocellular carcinoma (HCC) cells both in vitro and in vivo. This effect depended on a reduction of KLF6 expression in HCC cells. After incubation with either platelets or platelet granule contents, SMMC.7721 and HepG2 cells exhibited significant increases in proliferation and decreases in apoptosis. However, no effect was observed when incubating cancer cells with resuspended activated platelet pellet which exhausted of releasates. Platelet releasates also increased the population of HCC cells in the S and G2/M phases of the cell cycle and reduced the cell population in the G0/G1 phase. Moreover, knocking down KLF6 expression significantly diminished the platelet-mediated enhancement of HCC growth. In addition, blocking TGF-β signaling with the TGF-β receptor inhibitor SB431542 counteracted the effect of platelets on KLF6 expression and proliferation of HCC cells. Based on these findings, we conclude that platelet releasates, especially TGF-β, promote the proliferation of SMMC.7721 and HepG2 cells by decreasing expression of KLF6. This discovery identifies a potential new therapeutic target for the prevention and treatment of hepatocellular carcinoma.

10.1038/s41598-017-02801-1

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Antiplatelet activity of loureirin A by attenuating Akt phosphorylation: In vitro studies

European Journal of Pharmacology (2014)

Hong-Zhen Hao Ao‐Di He Dao-Chun Wang Zhao Yin Yajun Zhou

10.1016/j.ejphar.2014.10.059

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Antiplatelet activity of chrysin via inhibiting platelet αIIbβ3‐mediated signaling pathway

Molecular Nutrition & Food Research (2016)

Gang Liu Wen Xie Ao‐Di He Xingwen Da Minglu Liang

Scope Propolis is thought to help prevent thrombotic and related cardiovascular diseases in humans. Chrysin, a bioflavonoids compound found in high levels in propolis and in honey, has been reported to possess antiplatelet activity. However, the mechanism by which it inhibits platelet function is unclear. Methods and results The effects of chrysin on agonist‐activated platelet‐aggregation, granule‐secretion, and integrin αIIbβ3 activation were examined. Its effects on the phosphorylation of Akt, GSK3β, MAPKs, and several proteins of the glycoprotein VI (GPVI) signaling pathway were also studied on collaged‐activated platelets. In addition, human platelet spreading on immobilized fibrinogen was also tested. We found that chrysin dose dependently inhibited platelet aggregation and granule secretion induced by collagen, as well as platelet aggregation induced by ADP, thrombin, and U46619. Chrysin also markedly reduced the number of adherent platelets and the single platelet spreading area on immobilized fibrinogen. Biochemical analysis revealed that chrysin inhibited collagen‐induced activation of Syk, PLCγ2, PKC, as well as the phosphorylation of Akt and ERK1/2. Additionally, chrysin attenuated phosphorylation of molecules such as FcγRIIa, FAK, Akt, and GSK3β in platelet spreading on immobilized fibrinogen. Conclusions Our findings indicate that chrysin suppresses not only integrin αIIbβ3‐mediated “inside‐out” signaling, but also the “outside‐in” signal transmission. This implies that chrysin may represent a potential candidate for an antiplatelet agent.

Chrysin

Clot retraction

10.1002/mnfr.201500801

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