更新于：2024-11-01

complement factor x P-sel

更新于：2024-11-01

基本信息

关联

项与 complement factor x P-sel 相关的药物

IHP-102

靶点

P-sel x complement factor

作用机制

P-sel调节剂 [+1]

在研机构

IHP Therapeutics, Inc. [+1]

原研机构

IHP Therapeutics, Inc. [+1]

在研适应症

血管闭塞危机 [+1]

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

IHP-101

靶点

P-sel x complement factor

作用机制

P-sel调节剂 [+1]

在研机构

IHP Therapeutics, Inc.

原研机构

IHP Therapeutics, Inc.

在研适应症

实体瘤

非在研适应症-

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 complement factor x P-sel 相关的临床结果

登录后查看更多信息

100 项与 complement factor x P-sel 相关的转化医学

登录后查看更多信息

0 项与 complement factor x P-sel 相关的专利（医药）

登录后查看更多信息

项与 complement factor x P-sel 相关的文献（医药）

2013-01-01·American journal of blood research

Aging- and activation-induced platelet microparticles suppress apoptosis in monocytic cells and differentially signal to proinflammatory mediator release.

Article

作者: Weber, Christian ; Cauwenberghs, Sandra ; Koenen, Rory R ; Feijge, Marion Ah ; Vasina, Elena M ; Staudt, Mareike ; Heemskerk, Johan Wm

BACKGROUNDPlatelet microparticles (PM) are the most abundant cell-derived microparticles in the blood, and accumulate in thrombo-inflammatory diseases. Platelets produce PM upon aging via an apoptosis-like process and by activation with strong agonists. We previously showed that long-term treatment of monocytic cells with apoptosis-induced PM (PMap) promotes their differentiation into resident macrophages. Here we investigated shorter term effects of various types of PM on monocyte signalling and function.METHODS AND RESULTSFlow cytometry and scanning electron microscopy revealed that PM formed upon platelet aging (PMap) or ultra-sonication (PMsonic) expressed activated αIIbβ3 integrins and tended to assemble into aggregates. In contrast, PM formed upon platelet activation with thrombin (PMthr) or Ca(2+) ionophore (PMiono) had mostly non-activated αIIbβ3 and little aggregate formation, but had increased CD63 expression. PM from activated and sonicated platelets expressed phosphatidylserine at their surface, while only the latter were enriched in the receptors CD40L and CX3CR1. All PM types expressed P-selectin, interacted with monocytic cells via this receptor, and were internalised into these cells. The various PM types promoted actin cytoskeletal rearrangements and hydrogen peroxide production by monocytic cells. Markedly, both aging- and activation-induced PM types stimulated the phosphoinositide 3-kinase/Akt pathway, suppressing apoptosis induced by several agonists, in a P-selectin-dependent manner. On the other hand, the PM types differentially influenced monocyte signalling in eliciting Ca(2+) fluxes (particularly PMap) and in releasing secondary mediators (complement factor C5a with PMap, and pro-inflammatory tumour necrosis factor-α with PMthr).CONCLUSIONSIn spite of their common anti-apoptotic potential via Akt activation, aging- and activation-induced PM cause different Ca(2+) signalling events and mediator release in monocytic cells. By implication, aging and activated platelets may modulate monocyte function in different way by the shedding of different PM types.

2011-04-01·Annals of Biomedical Engineering2区 · 工程技术

Hemocompatibility of Silicon-Based Substrates for Biomedical Implant Applications

2区 · 工程技术

Article

作者: William H. Fissell ; Shuvo Roy ; Tejal A. Desai ; Roger E. Marchant ; Rachel Lowe ; Lingyan Li ; Lalitha Muthusubramaniam

Silicon membranes with highly uniform nanopore sizes fabricated using microelectromechanical systems (MEMS) technology allow for the development of miniaturized implants such as those needed for renal replacement therapies. However, the blood compatibility of silicon has thus far been an unresolved issue in the use of these substrates in implantable biomedical devices. We report the results of hemocompatibility studies using bare silicon, polysilicon, and modified silicon substrates. The surface modifications tested have been shown to reduce protein and/or platelet adhesion, thus potentially improving biocompatibility of silicon. Hemocompatibility was evaluated under four categories-coagulation (thrombin-antithrombin complex, TAT generation), complement activation (complement protein, C3a production), platelet activation (P-selectin, CD62P expression), and platelet adhesion. Our tests revealed that all silicon substrates display low coagulation and complement activation, comparable to that of Teflon and stainless steel, two materials commonly used in medical implants, and significantly lower than that of diethylaminoethyl (DEAE) cellulose, a polymer used in dialysis membranes. Unmodified silicon and polysilicon showed significant platelet attachment; however, the surface modifications on silicon reduced platelet adhesion and activation to levels comparable to that on Teflon. These results suggest that surface-modified silicon substrates are viable for the development of miniaturized renal replacement systems.