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纳米海绵 1

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Abivertinib inhibits megakaryocyte differentiation and platelet biogenesis

《医学前沿（英文）》 2022年 第16卷 第3期   页码 416-428 doi: 10.1007/s11684-021-0838-5

摘要： Abivertinib, a third-generation tyrosine kinase inhibitor, is originally designed to target epidermal growth factor receptor (EGFR)-activating mutations. Previous studies have shown that abivertinib has promising antitumor activity and a well-tolerated safety profile in patients with non-small-cell lung cancer. However, abivertinib also exhibited high inhibitory activity against Bruton’s tyrosine kinase and Janus kinase 3. Given that these kinases play some roles in the progression of megakaryopoiesis, we speculate that abivertinib can affect megakaryocyte (MK) differentiation and platelet biogenesis. We treated cord blood CD34+ hematopoietic stem cells, Meg-01 cells, and C57BL/6 mice with abivertinib and observed megakaryopoiesis to determine the biological effect of abivertinib on MK differentiation and platelet biogenesis. Our in vitro results showed that abivertinib impaired the CFU-MK formation, proliferation of CD34+ HSC-derived MK progenitor cells, and differentiation and functions of MKs and inhibited Meg-01-derived MK differentiation. These results suggested that megakaryopoiesis was inhibited by abivertinib. We also demonstrated in vivo that abivertinib decreased the number of MKs in bone marrow and platelet counts in mice, which suggested that thrombopoiesis was also inhibited. Thus, these preclinical data collectively suggested that abivertinib could inhibit MK differentiation and platelet biogenesis and might be an agent for thrombocythemia.

关键词： abivertinib     Btk inhibitor     platelet     megakaryocyte     megakaryopoiesis     thrombopoiesis    

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Platelet-rich plasma: combinational treatment modalities for musculoskeletal conditions

null

《医学前沿（英文）》 2018年 第12卷 第2期   页码 139-152 doi: 10.1007/s11684-017-0551-6

摘要：

Current research on common musculoskeletal problems, including osteoarticular conditions, tendinopathies, and muscle injuries, focuses on regenerative translational medicine. Platelet-rich plasma therapies have emerged as a potential approach to enhance tissue repair and regeneration. Platelet-rich plasma application aims to provide supraphysiological concentrations of platelets and optionally leukocytes at injured/pathological tissues mimicking the initial stages of healing. However, the efficacy of platelet-rich plasma is controversial in chronic diseases because patients’ outcomes show partial improvements. Platelet-rich plasma can be customized to specific conditions by selecting the most appropriate formulation and timing for application or by combining platelet-rich plasma with synergistic or complementary treatments. To achieve this goal, researchers should identify and enhance the main mechanisms of healing. In this review, the interactions between platelet-rich plasma and healing mechanisms were addressed and research opportunities for customized treatment modalities were outlined. The development of combinational platelet-rich plasma treatments that can be used safely and effectively to manipulate healing mechanisms would be valuable and would provide insights into the processes involved in physiological healing and pathological failure.

关键词： regenerative medicine     joint conditions     muscle injuries     platelet rich plasma     tendinopathy     healing mechanisms    

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Engineering platelet-mimicking drug delivery vehicles

Quanyin Hu, Hunter N. Bomba, Zhen Gu

《化学科学与工程前沿（英文）》 2017年 第11卷 第4期   页码 624-632 doi: 10.1007/s11705-017-1614-6

摘要： Platelets dynamically participate in various physiological processes, including wound repair, bacterial clearance, immune response, and tumor metastasis. Recreating the specific biological features of platelets by mimicking the structure of the platelet or translocating the platelet membrane to synthetic particles holds great promise in disease treatment. This review highlights recent advancements made in the platelet-mimicking strategies. The future opportunities and translational challenges are also discussed.

关键词： drug delivery     platelets     nanomedicine     bio-inspired     biomimetic    

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Platelet membrane-based and tumor-associated platelet- targeted drug delivery systems for cancer therapy

Yinlong Zhang, Guangna Liu, Jingyan Wei, Guangjun Nie

《医学前沿（英文）》 2018年 第12卷 第6期   页码 667-677 doi: 10.1007/s11684-017-0583-y

摘要： Platelets have long been known to play critical roles in hemostasis by clumping and clotting blood vessel injuries. Recent experimental evidence strongly indicates that platelets can also interact with tumor cells by direct binding or secreting cytokines. For example, platelets have been shown to protect circulating cancer cells in blood circulation and to promote tumor metastasis. In-depth understanding of the role of platelets in cancer progression and metastasis provides promising approaches for platelet biomimetic drug delivery systems and functional platelet-targeting strategies for effective cancer treatment. This review highlights recent progresses in platelet membrane-based drug delivery and unique strategies that target tumor-associated platelets for cancer therapy. The paper also discusses future development opportunities and challenges encountered for clinical translation.

关键词： platelet-mimicking delivery systems     tumor-associated platelets     cancer therapy     EPR effect    

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The relationship between platelet-derived growth factor expression and angiogenesis/lymphangiogenesis

Guocheng LIU MD, Shouhua YANG MD, Zehua WANG MD,

《医学前沿（英文）》 2009年 第3卷 第4期   页码 447-451 doi: 10.1007/s11684-009-0082-x

摘要： This paper is aimed to examine if changes in platelet-derived growth factor (PDGF) expression at different stages of cervical cancer are related to the variation in blood vessel density (BVD) and lymphatic vessel density (LVD) to evaluate the relationship between PDGF expression and stages and metastasis of cervical cancer. Polymerase chain reaction (PCR) and RT-PCR were used to detect the expression levels of PDGF in 45 cervical cancer tissue samples (the experimental group). The samples were immunohistochemically stained with monoclonal antibodies D2-40 and CD34, and BVD and LVD were measured. The expressions of PDGF-A, -B, and- D were all higher in the experimental group than in the control group (<0.05); no significant difference was found in the expression of PDGF-C between the experimental group and the control group (>0.05). PDGF-A and -B expression was positively related with BVD and LVD (<0.01, R= 0.49, 0.527, 0.327, 0.68). The expression levels of PDGF-C and -D were not significantly related with BVD and LVD. At the early stage of cervical cancer, BVD and LVD were significantly higher than in the controls (<0.01). The BVD and LVD in tissues in the surrounding areas of cervical cancer were significantly higher than in tissues at cancer center, and LVD was related to lymph node metastasis (<0.001). BVD and LVD were not associated with the differentiation and pathological stages of cervical cancer. The expressions of PDGF-A, -B, and -D in cervical cancer were closely related with the clinical stages of cervical cancer. PDGF-A and -B were intimately associated with the lymph node metastasis and prognosis of cervical cancer.

关键词： cervical cancer     lymphatic vessel density     blood vessel density     platelet-derived growth factor    

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Anti-β glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two

null

《医学前沿（英文）》 2016年 第10卷 第1期   页码 76-84 doi: 10.1007/s11684-015-0426-7

摘要：

Anti-β2 glycoprotein I (anti-β2GP I ) antibodies are important contributors to thrombosis, especially in patients with antiphospholipid syndrome (APS). However, the mechanism by which anti-β2GP I antibodies are involved in the pathogenesis of thrombosis is not fully understood. In this report, we investigated the role of anti-β2GP I antibodies in complexes with β2GP I as mediators of platelet activation, which can serve as a potential source contributing to thrombosis. We examined the involvement of the apolipoprotein E receptor 2' (apoER2') and glycoprotein I ba (GP I bα) in platelet activation induced by the anti-β2GP I /β2GP I complex. The interaction between the anti-β2GP I /β2GP I complex and platelets was examined using in vitro methods, in which the Fc portion of the antibody was immobilized using protein A coated onto a microtiter plate. Platelet activation was assessed by measuring GP II b/ III a activation and P-selectin expression and thromboxane B2 production as well as p38 mitogen-activated protein kinase phosphorylation. Our results revealed that the anti-β2GP I /β2GP I complex was able to activate platelets, and this activation was inhibited by either the anti-GP I bα antibody or the apoER2' inhibitor. Results showed that the anti-β2GP I /β2GP I complex induced platelet activation via GP I bα and apoER2', which may then contribute to the prothrombotic tendency in APS patients.

关键词： anti-β2GP I /β2GP I complex     platelet     GP I bα     apoER2'     thrombosis    

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polycarbonateurethane surface with poly(ethylene glycol) monoacrylate and phosphorylcholine glyceraldehyde for anti-platelet

Jing YANG,Juan LV,Bin GAO,Li ZHANG,Dazhi YANG,Changcan SHI,Jintang GUO,Wenzhong LI,Yakai FENG

《化学科学与工程前沿（英文）》 2014年 第8卷 第2期   页码 188-196 doi: 10.1007/s11705-014-1414-1

摘要： Poly(ethylene glycol) monoacrylate (PEGMA) is grafted onto polycarbonateurethane (PCU) surface via ultraviolet initiated photopolymerization. The hydroxyl groups of poly(PEGMA) on the surface react with one NCO group of isophorone diisocyanate (IPDI) and another NCO group of IPDI is then hydrolyzed to form amino terminal group, which is further grafted with phosphorylcholine glyceraldehyde to establish a biocompatible hydrophilic structure on the surface. Fourier transform infrared spectroscopy and X-ray photoelectron spectroscopy confirm the successful grafting of both PEG and phosphorylcholine functional groups on the surface. The decrease of the water contact angle for the modified film is caused by synergic effect of PEG and phosphorylcholine, which both have the high hydrophilicity. Furthermore, the number of platelets adhered is relative low on the synergetically modified PCU film compared with the PCU film modified only by poly(PEGMA). Our synergic modification method using both PEG and phosphorylcholine may be applied in surface modification of blood-contacting biomaterials and some relevant devices.

关键词： poly(ethylene glycol) monoacrylate     phosphorylcholine     polycarbonateurethane     surface modification     anti-platelet adhesion     biomaterials    

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The change of serum leptin and its relationship with platelet membrane glycoprotein Ib in patients with

XIA Dasheng, SONG Yanqiu, LI Chao, ZHANG Feng, WEI Minxin

《医学前沿（英文）》 2007年 第1卷 第4期   页码 352-355 doi: 10.1007/s11684-007-0067-6

摘要： The aim of this paper was to investigate the change of serum leptin and its relationship with platelet membrane glycoprotein Ib (GP Ib) in patients with coronary heart disease (CHD). The enrolled included 50 patients with CHD (CHD group) and 30 patients without CHD (control group) who were diagnosed by coronary angiography. The positive percentage and the average fluorescence intensity of platelet membrane GP Ib were detected by full-blood flow cytometry. Serum leptin was detected by enzyme linked immunosorbent assay. The positive percentage and the average fluorescence intensity of platelet membrane GP Ib in the CHD group were significantly lower than those in the control group (<0.05). After correcting the differences of systolic blood pressure, body mass index (BMI), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), fasting glucose, PPBS, fasting insulin and quantitative insulin sensitive index, serum leptin level in the CHD group was significantly higher than that in the control group (<0.05). Single factor correlative analysis revealed that serum leptin in CHD patients was negatively correlated with the average fluorescence intensity of platelet membrane GP Ib (<0.05). Multifactorial stepwise regression analysis showed that serum leptin in CHD patients was independently negatively correlated with the average fluorescence intensity of platelet membrane GP Ib (<0.05). Logistic analysis demonstrated that serum leptin was independently correlated with the risk of CHD (<0.05). Hyperleptinemia was verified in CHD patients. The increase of serum leptin could affect blood platelet activation. Hyperleptinemia may play an important role in the pathogenesis of CHD.
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Expression of protease-activated receptors on platelets in healthy individuals

Rui ZHU, Lin SHEN

《医学前沿（英文）》 2009年 第3卷 第2期   页码 236-239 doi: 10.1007/s11684-009-0040-7

摘要： This study aimed to investigate the expression of protease-activated receptors (PARs) on platelets in healthy individuals and preliminarily elucidate physiological functions of PARs. Thirty healthy volunteers, who did not take any anticoagulants and antiplatelet agents within 10 days before the examination, were recruited. Fasting venous blood (5 mL) was taken from the medial cubital vein in each individual and platelet-rich plasma (PRP) was prepared. The expression of PAR1 mRNA and PAR4 mRNA in PRP was determined by RT-PCR analysis. The results showed that the average levels of PAR1 mRNA and PAR4 mRNA on platelets in healthy individuals were 0.1601 ± 0.0269 and 0.1073 ± 0.0194 respectively. In combination with literature analysis, it was concluded that the thrombin signaling pathway plays a vital role in the development of hemostasis and thrombosis, and the selective PARs antagonist has the potential for extensive application in clinical practice.

关键词： protease-activated receptors     platelet    

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Involvement of p38 mitogen-activated protein kinase in the regulation of platelet-derived growth factor

GONG Xiaowei, WEI Jie, LI Yusheng, CHENG Weiwei, DENG Peng, JIANG Yong

《医学前沿（英文）》 2007年 第1卷 第3期   页码 248-252 doi: 10.1007/s11684-007-0047-x

摘要： The aim of this study was to investigate the role of p38 mitogen-activated protein kinase (MAPK) in cell migration induced by platelet-derived growth factor (PDGF). Western blot was performed to detect the phosphorylation of p38 in NIH3T3 cells treated with PDGF. A Transwell cell migration system was used to determine the effects of PDGF treatment on the migration of NIH3T3 cells and the influence of deficiency on this process in a gene knockout (p38) mouse embryonic fibroblast cell line. On the stimulation of PDGF, the migration of NIH3T3 cells was significantly increased (〈0.001) compared to the control and p38 MAP kinase was simultaneously phosphorylated. Furthermore, the PDGF-induced cell migration was significantly blocked in gene knockout (p38) mouse embryonic fibroblasts (MEFs) (〈0.001) as compared with the wild type cells (p38). p38 MAPK plays an important role in the regulation of cell migration induced by PDGF.

关键词： control     stimulation     mitogen-activated     growth factor     process    

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Anti-β2GPI/β2GPI complexes induce platelet activation and promote thrombosis via

Wenjing Zhang, Caijun Zha, Xiumin Lu, Ruichun Jia, Fei Gao, Qi Sun, Meili Jin, Yanhong Liu

《医学前沿（英文）》 2019年 第13卷 第6期   页码 680-689 doi: 10.1007/s11684-018-0673-5

摘要： Anti- glycoprotein I (anti- GPI) antibodies are important contributors to the development of thrombosis. Anti- GPI antibody complexes with GPI are well known to activate monocytes and endothelial cells via the intracellular NF- B pathway with prothrombotic implications. By contrast, the interaction of anti- GPI/ GPI complexes with platelets has not been extensively studied. The p38 mitogen-activated protein kinase (MAPK) pathway has been recognized to be an important intracellular signaling pathway in the coagulation cascade and an integral component of arterial and venous thrombosis. The present study reveals that levels of anti- GPI/ GPI complexes in sera are positively associated with p38MAPK phosphorylation of platelets in thrombotic patients. Furthermore, SB203580 inhibits anti- GPI/ GPI complex-induced platelet activation. Thrombus formation decreased in mice after treatment with anti- GPI/ GPI complexes. In conclusion, p38MAPK may be a treatment target for anti- GPI antibody-associated thrombotic events.

关键词： anti-   

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工程化仿生血小板膜包覆纳米颗粒阻断金黄色葡萄球菌的细胞毒性并防止致命的全身感染 Article

Jwa-Kyung Kim, Satoshi Uchiyama, Hua Gong, Alexandra Stream, Liangfang Zhang, Victor Nizet

《工程（英文）》 2021年 第7卷 第8期   页码 1149-1156 doi: 10.1016/j.eng.2020.09.013

摘要：

金黄色葡萄球菌（S. aureus）是一种常见的人类病原体，它可以引发严重的侵袭性感染，如菌血症、败血症和心内膜炎，具有较高的发病率和死亡率。然而由于细菌的抗生素耐药性增强，如耐甲氧西林金黄色葡萄球菌（MRSA），加剧了此类细菌的发病率和死亡率。金黄色葡萄球菌的发病机制是由毒素的分泌推动的，如膜损伤孔α毒素，它有不同的细胞靶点，包括上皮细胞、内皮细胞、白细胞和血小板。本文采用人体血小板膜包覆纳米颗粒（PNP）作为一种仿生诱饵策略，来中和金黄色葡萄球菌的毒素，并维持宿主细胞的防御功能。血小板膜包覆纳米颗粒保护血小板免受由金黄色葡萄球菌毒素带来的损伤，维持血小板活化和杀菌活性。血小板膜包覆纳米颗粒也同样保护巨噬细胞免受由金黄色葡萄球菌毒素带来的损伤，支持巨噬细胞进行氧化迸发、产生一氧化氮和维持其杀菌活性，并减少耐甲氧西林金黄色葡萄球菌诱导的中性粒细胞胞外杀菌网络。在感染系统性耐甲氧西林金黄色葡萄球菌的小鼠模型中，血小板膜包覆纳米颗粒制剂减少了血液中的细菌数量并防止小鼠发生死亡。总之，目前的研究结果证明了血小板膜包覆纳米颗粒的治疗优点，如中和毒素、保护细胞和增加宿主对侵袭性金黄色葡萄球菌感染的抵抗力。

关键词： 纳米颗粒     纳米海绵     血小板     金黄色葡萄球菌     细菌毒素     败血症    

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Plasma-enabled healing of graphene nano-platelets layer

Xiuqi Fang, Carles Corbella, Denis B. Zolotukhin, Michael Keidar

《化学科学与工程前沿（英文）》 2019年 第13卷 第2期   页码 350-359 doi: 10.1007/s11705-018-1787-7

摘要： Graphene platelet networks (GPNs) were deposited onto silicon substrates by means of anodic arc discharge ignited between two graphite electrodes. Substrate temperature and pressure of helium atmosphere were optimized for the production of the carbon nanomaterials. The samples were modified or destroyed with different methods to mimic typical environments responsible of severe surface degradation. The emulated conditions were performed by four surface treatments, namely thermal oxidation, substrate overheating, exposition to glow discharge, and metal coating due to arc plasma. In the next step, the samples were regenerated on the same substrates with identical deposition technique. Damaging and re-growth of GPN samples were systematically characterized by scanning electron microscopy and Raman spectroscopy. The full regeneration of the structural and morphological properties of the samples has proven that this healing method by arc plasma is adequate for restoring the functionality of 2D nanostructures exposed to harsh environments.

关键词： graphene platelet networks     anodic arc discharge     plasma healing     scanning electron microscopy     Raman spectroscopy    

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标题 作者 时间 类型 操作

Abivertinib inhibits megakaryocyte differentiation and platelet biogenesis

期刊论文

Platelet-rich plasma: combinational treatment modalities for musculoskeletal conditions

null

期刊论文

Engineering platelet-mimicking drug delivery vehicles

Quanyin Hu, Hunter N. Bomba, Zhen Gu

期刊论文

Platelet membrane-based and tumor-associated platelet- targeted drug delivery systems for cancer therapy

Yinlong Zhang, Guangna Liu, Jingyan Wei, Guangjun Nie

期刊论文

The relationship between platelet-derived growth factor expression and angiogenesis/lymphangiogenesis

Guocheng LIU MD, Shouhua YANG MD, Zehua WANG MD,

期刊论文

Anti-β glycoprotein I antibodies in complex with β2 glycoprotein I induce platelet activation via two

null

期刊论文

polycarbonateurethane surface with poly(ethylene glycol) monoacrylate and phosphorylcholine glyceraldehyde for anti-platelet

Jing YANG,Juan LV,Bin GAO,Li ZHANG,Dazhi YANG,Changcan SHI,Jintang GUO,Wenzhong LI,Yakai FENG

期刊论文

The change of serum leptin and its relationship with platelet membrane glycoprotein Ib in patients with

XIA Dasheng, SONG Yanqiu, LI Chao, ZHANG Feng, WEI Minxin

期刊论文

Expression of protease-activated receptors on platelets in healthy individuals

Rui ZHU, Lin SHEN

期刊论文

Involvement of p38 mitogen-activated protein kinase in the regulation of platelet-derived growth factor

GONG Xiaowei, WEI Jie, LI Yusheng, CHENG Weiwei, DENG Peng, JIANG Yong

期刊论文

Anti-β2GPI/β2GPI complexes induce platelet activation and promote thrombosis via

Wenjing Zhang, Caijun Zha, Xiumin Lu, Ruichun Jia, Fei Gao, Qi Sun, Meili Jin, Yanhong Liu

期刊论文

工程化仿生血小板膜包覆纳米颗粒阻断金黄色葡萄球菌的细胞毒性并防止致命的全身感染

Jwa-Kyung Kim, Satoshi Uchiyama, Hua Gong, Alexandra Stream, Liangfang Zhang, Victor Nizet

期刊论文

Plasma-enabled healing of graphene nano-platelets layer

Xiuqi Fang, Carles Corbella, Denis B. Zolotukhin, Michael Keidar

期刊论文