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Transplantation of human neural stem/progenitor cells overexpressing galectin-1 improves functional recovery from focal brain ischemia in the mongolian gerbil

DOI: 10.1186/1756-6606-4-35

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Abstract:

Stem cell-based therapies have been performed in various clinical settings, although many lack scientific evidence of their effectiveness [1]. Among stem cell-based therapies, transplantation of human neural stem/progenitor cells (hNSPCs) is relatively well substantiated by peer-reviewed literatures [2-8]. One reason underlying the relative success of hNSPCs-transplantation is its low occurrence of tumor formation, which is a clear advantage compared with transplantation of embryonic stem cells or their derivatives [9]. Therefore, we have been examining hNSPCs-transplantation in various preclinical animal models and have shown that hNSPCs-transplantation enhances functional recovery following brain ischemia [10] and spinal cord injury (SCI) [11].Brain ischemia, which is caused by occlusion of a cerebral artery, leads to focal tissue loss and death of multiple neuronal cell types within and around the ischemic region. Patients with brain ischemia exhibit persistent motor, sensory or cognitive impairments, which have devastating effects on their quality of life. Apart from acute thrombolysis, which can be used in only a minority of cases, there is still no effective treatment to promote functional recovery after brain ischemia.hNSPCs can generate all principle cell types (i.e., neurons, astrocytes and oligodendrocytes) in the brain and therefore have great therapeutic potential in severe neurological diseases, including brain ischemia [6,12], which induce death of various cell types [13,14]. hNSPCs can be propagated in large quantities for long-term without a notable loss of the ability to proliferate and differentiate [15]. Therefore, cultured hNSPCs are a promising cell source to treat brain diseases.We previously showed that transplantation of cultured hNSPCs reduced infarct volume and improved functional prognosis in a rodent model of brain ischemia [10]. In the damaged brains of the model animals, hNSPCs differentiated into mature neurons within the ischemic regi

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