Bone marrow stromal cells promote neuroplasticity of cerebral ischemic rats via a phosphorylated CRMP2-mediated mechanism

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• 作者：Xiang He^a ; ¹ ; Ling Jiang^a ; ¹ ; Qi-qin Dan^a ; Qiang Lv^a ; Yue Hu^a ; Jia Liu^b ; Shu-fen Wang^c ; ^{wsf66@hotmail.com} ; Ting-hua Wang^a ; ^b ; ^{tinghua_neuron@263.net}
• 关键词：CRMP2 ; collapsin response mediator protein 2 ; BMSCs ; bone marrow stromal cells ; MCAO ; middle cerebral artery occlusion ; SYP ; synaptophysin ; GSK3β ; glycogen synthase kinase 3 beta ; CDK5 ; cyclin-dependent kinase 5 ; mNSS ; modified neurological severity scores ; MEPs ; motor-evoked potentials ; SEPs ; somatosensory-evoked potentials ; CNTF ; ciliary neurotrophic factor ; PDGFB ; platelet derived growth factor subunit B ; TGFB1 ; transforming growth factor beta 1 ; NGF ; nerve growth factor ; BDNF ; brain-derived
• 刊名：Behavioural Brain Research
• 出版年：2017
• 出版时间：1 March 2017
• 年：2017
• 卷：320
• 期：Complete
• 页码：494-503
• 全文大小：3134 K
• 卷排序：320

文摘

The neuroplasticity following cerebral ischemia is ameliorated by BMSCs transplant. The mechanism may be associated with the expressional change of phosphorylated collapsin response mediator protein 2 (p-CRMP2). The secretion of neurotrophins and the activation of signaling pathways by BMSCs may affect the expression of p-CRMP2. BMSCs treatment could promote neuroplasticity impared by brain ischemic injury.