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Stem cell therapy for abrogating stroke-induced neuroinflammation and relevant secondary cell death mechanisms
Progress in Neurobiology ( IF 6.7 ) Pub Date : 2017-07-23 , DOI: 10.1016/j.pneurobio.2017.07.004
Connor Stonesifer , Sydney Corey , Shaila Ghanekar , Zachary Diamandis , Sandra A. Acosta , Cesar V. Borlongan

Ischemic stroke is a leading cause of death worldwide. A key secondary cell death mechanism mediating neurological damage following the initial episode of ischemic stroke is the upregulation of endogenous neuroinflammatory processes to levels that destroy hypoxic tissue local to the area of insult, induce apoptosis, and initiate a feedback loop of inflammatory cascades that can expand the region of damage. Stem cell therapy has emerged as an experimental treatment for stroke, and accumulating evidence supports the therapeutic efficacy of stem cells to abrogate stroke-induced inflammation. In this review, we investigate clinically relevant stem cell types, such as hematopoietic stem cells (HSCs), mesenchymal stem cells (MSCs), endothelial progenitor cells (EPCs), very small embryonic-like stem cells (VSELs), neural stem cells (NSCs), extraembryonic stem cells, adipose tissue-derived stem cells, breast milk-derived stem cells, menstrual blood-derived stem cells, dental tissue-derived stem cells, induced pluripotent stem cells (iPSCs), teratocarcinoma-derived Ntera2/D1 neuron-like cells (NT2N), c-mycER(TAM) modified NSCs (CTX0E03), and notch-transfected mesenchymal stromal cells (SB623), comparing their potential efficacy to sequester stroke-induced neuroinflammation and their feasibility as translational clinical cell sources. To this end, we highlight that MSCs, with a proven track record of safety and efficacy as a transplantable cell for hematologic diseases, stand as an attractive cell type that confers superior anti-inflammatory effects in stroke both in vitro and in vivo. That stem cells can mount a robust anti-inflammatory action against stroke complements the regenerative processes of cell replacement and neurotrophic factor secretion conventionally ascribed to cell-based therapy in neurological disorders.



中文翻译:

干细胞疗法可消除中风诱发的神经炎症及相关的继发细胞死亡机制

缺血性中风是全球范围内主要的死亡原因。缺血性脑卒中发作后介导神经系统损伤的关键继发细胞死亡机制是内源性神经炎症过程上调至破坏损伤部位局部缺氧组织,诱导细胞凋亡并启动炎症级联反应反馈回路的水平损坏区域。干细胞疗法已经作为中风的实验方法出现,越来越多的证据支持干细胞消除中风引起的炎症的治疗功效。在这篇综述中,我们研究了临床相关的干细胞类型,例如造血干细胞(HSC),间充质干细胞(MSC),内皮祖细胞(EPC),非常小的胚胎样干细胞(VSEL),神经干细胞( NSC),胚外干细胞,脂肪组织干细胞,母乳来源干细胞,月经血来源干细胞,牙科组织来源干细胞,诱导多能干细胞(iPSC),畸胎瘤来源的Ntera2 / D1神经元样细胞(NT2N),c-mycER(TAM)修饰的NSC(CTX0E03)和Notch转染的间充质基质细胞(SB623),比较了它们对螯合卒中诱导的神经炎症的潜在功效以及作为转化临床细胞来源的可行性。为此,我们着重指出,MSC作为血液系统疾病的可移植细胞具有良好的安全性和有效性,并具有良好的往绩记录,是一种有吸引力的细胞类型,在中风中均具有出色的抗炎作用 牙科组织来源的干细胞,诱导性多能干细胞(iPSC),畸胎瘤来源的Ntera2 / D1神经元样细胞(NT2N),c-mycER(TAM)修饰的NSC(CTX0E03)和缺口转染的间充质基质细胞(SB623) ),比较了它们对隔离性中风诱发的神经炎症的潜在疗效,以及它们作为转化临床细胞来源的可行性。为此,我们着重指出,MSC作为血液系统疾病的可移植细胞具有良好的安全性和有效性,并具有良好的往绩记录,是一种有吸引力的细胞类型,在中风中均具有出色的抗炎作用 牙科组织来源的干细胞,诱导性多能干细胞(iPSC),畸胎瘤来源的Ntera2 / D1神经元样细胞(NT2N),c-mycER(TAM)修饰的NSC(CTX0E03)和缺口转染的间充质基质细胞(SB623) ),比较了它们对隔离性中风诱发的神经炎症的潜在疗效,以及它们作为转化临床细胞来源的可行性。为此,我们着重指出,MSC作为血液系统疾病的可移植细胞具有良好的安全性和有效性,并具有良好的往绩记录,是一种有吸引力的细胞类型,在中风中均具有出色的抗炎作用 比较了它们对隔离性中风诱发的神经炎症的潜在疗效,以及它们作为转化型临床细胞来源的可行性。为此,我们着重指出,MSC作为血液系统疾病的可移植细胞具有良好的安全性和有效性,并具有良好的往绩记录,是一种有吸引力的细胞类型,在中风中均具有出色的抗炎作用 比较了它们对隔离性中风诱发的神经炎症的潜在疗效,以及它们作为转化型临床细胞来源的可行性。为此,我们着重指出,MSC作为血液系统疾病的可移植细胞具有良好的安全性和有效性,并具有良好的往绩记录,是一种有吸引力的细胞类型,在中风中均具有出色的抗炎作用体外体内。该干细胞可以对中风起强有力的抗炎作用,补充了通常归因于神经系统疾病的基于细胞的治疗所产生的细胞置换和神经营养因子分泌的再生过程。

更新日期:2017-07-23
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