Mesenchymal stem cell-based treatments for stroke, neural trauma, and heat stroke.

Mesenchymal stem cell-based treatments for stroke, neural trauma, and heat stroke.
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DOI:
10.1002/brb3.526
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发表时间:
2016-10
期刊:
影响因子:
3.1
通讯作者:
Lin, Mao-Tsun
Lin, Mao-Tsun
中科院分区:
心理学4区
文献类型:
--
作者:
Hsuan, Yogi Chang-Yo;Lin, Cheng-Hsien;Chang, Ching-Ping;Lin, Mao-Tsun

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间充质干细胞(MSC)移植已被报道,以改善神经损伤后的神经功能。已经确定了许多涉及MSC治疗相关神经保护的生理和分子机制。综述了与MSC治疗和各种脑损伤(包括中风、神经创伤和中暑)有关的文章,这些文章是使用电子搜索(例如,PubMed),强调MSC治疗相关的神经保护机制。我们的目标是讨论MSC在治疗中风、神经创伤和中暑方面的有益作用的神经保护机制。 MSC疗法作为增强脑修复的手段是有希望的。细胞掺入到损伤组织中并不是MSC发挥有益作用的先决条件。旁分泌信号被认为是MSC治疗脑损伤的最重要的介质。MSC的多种作用机制包括增强血管生成和神经发生、免疫调节和抗炎作用。小胶质细胞是脑损伤过程中炎症级联反应的第一个来源。细胞因子,包括肿瘤坏死因子-α、白细胞介素-1 β和白细胞介素-6,在实验性脑损伤后由脑中的小胶质细胞显著产生。小胶质细胞的促炎M1表型与组织破坏相关,而小胶质细胞的抗炎M2表型促进修复和再生。MSC治疗可以通过抑制小胶质细胞M1表型的活性但增强小胶质细胞M2表型的活性来改善缺血性中风、神经创伤和中暑的结果。本综述为今后MSC治疗的合理设计提供了一个可测试的平台,为临床试验中靶向小胶质细胞介导的细胞因子提供了依据。来源于胎盘的MSC为干细胞治疗提供了一个很好的选择。虽然靶向小胶质细胞活化是减轻损伤负担的重要方法,但它不是唯一的方法。本次审查侧重于这一具体方面。
Mesenchymal stem cell (MSC) transplantation has been reported to improve neurological function following neural injury. Many physiological and molecular mechanisms involving MSC therapy‐related neuroprotection have been identified. A review is presented of articles that pertain to MSC therapy and diverse brain injuries including stroke, neural trauma, and heat stroke, which were identified using an electronic search (e.g., PubMed), emphasize mechanisms of MSC therapy‐related neuroprotection. We aim to discuss neuroprotective mechanisms that underlie the beneficial effects of MSCs in treating stroke, neural trauma, and heatstroke. MSC therapy is promising as a means of augmenting brain repair. Cell incorporation into the injured tissue is not a prerequisite for the beneficial effects exerted by MSCs. Paracrine signaling is believed to be the most important mediator of MSC therapy in brain injury. The multiple mechanisms of action of MSCs include enhanced angiogenesis and neurogenesis, immunomodulation, and anti‐inflammatory effects. Microglia are the first source of the inflammatory cascade during brain injury. Cytokines, including tumor necrosis factor‐α, interleukin‐1β, and interleukin‐6, are significantly produced by microglia in the brain after experimental brain injury. The proinflammatory M1 phenotype of microglia is associated with tissue destruction, whereas the anti‐inflammatory M2 phenotype of microglia facilitates repair and regeneration. MSC therapy may improve outcomes of ischemic stroke, neural trauma, and heatstroke by inhibiting the activity of M1 phenotype of microglia but augmenting the activity of M2 phenotype of microglia. This review offers a testable platform for targeting microglial‐mediated cytokines in clinical trials based upon the rational design of MSC therapy in the future. MSCs that are derived from the placenta provide a great choice for stem cell therapy. Although targeting the microglial activation is an important approach to reduce the burden of the injury, it is not the only one. This review focuses on this specific aspect.
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影响因子: 2.8
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CHANG, DM
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发表时间: 2004-10-01
期刊: STROKE
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发表时间: 2005-06-01
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期刊: NEUROREPORT
影响因子: 1.7
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