Cellular and Molecular Neurobiology Area, Group of Neuroscience of Antioquia, School of Medicine, SIU, University of Antioquia UdeA, Calle 70 No. 52-21, Medellin, Colombia.
Mol Neurobiol. 2017 Nov;54(9):6681-6696. doi: 10.1007/s12035-016-0162-2. Epub 2016 Oct 15.
Cerebral ischemia is a cerebrovascular episode that generates a high incidence of death and physical and mental disabilities worldwide. Excitotoxicity, release of free radicals, and exacerbated immune response cause serious complications in motor and cognitive areas during both short and long time frames post-ischemia. CDK5 is a kinase that is widely involved in the functions of neurons and astrocytes, and its over-activation is implicated in neurodegenerative processes. In this study, we evaluated the brain parenchymal response to the transplantation of CDK5-knockdown astrocytes into the somatosensory cortex after ischemia in rats. Male Wistar rats were subjected to the two-vessel occlusion (2VO) model of global cerebral ischemia and immediately transplanted with shCDK5miR- or shSCRmiR-transduced astrocytes or with untransduced astrocytes (Control). Our findings showed that animals transplanted with shCDK5miR astrocytes recovered motor and neurological performance better than with those transplanted with WT or shSCRmiR astrocytes. Cell transplantation produced an overall prevention of neuronal loss, and CDK5-knockdown astrocytes significantly increased the immunoreactivity (IR) of endogenous GFAP in branches surrounding blood vessels, accompanied by the upregulation of PECAM-1 IR in the walls of vessels in the motor and somatosensory regions and by an increase in Ki67 IR in the subventricular zone (SVZ), partially associated with the production of BDNF. Together, our data suggest that transplantation of shCDK5miR astrocytes protects the neurovascular unit in ischemic rats, allowing the motor and neurological function recovery.
脑缺血是一种脑血管事件,在全球范围内导致高死亡率和身心残疾。兴奋性毒性、自由基释放和免疫反应加剧会在缺血后短时间和长时间内导致运动和认知区域出现严重并发症。CDK5 是一种激酶,广泛参与神经元和星形胶质细胞的功能,其过度激活与神经退行性过程有关。在这项研究中,我们评估了 CDK5 敲低星形胶质细胞移植到大鼠缺血后体感皮层后的脑实质反应。雄性 Wistar 大鼠接受双侧颈总动脉结扎(2VO)全脑缺血模型,并立即移植 shCDK5miR-或 shSCRmiR 转导的星形胶质细胞或未转导的星形胶质细胞(对照)。我们的研究结果表明,与移植 WT 或 shSCRmiR 星形胶质细胞的动物相比,移植 shCDK5miR 星形胶质细胞的动物在运动和神经功能恢复方面更好。细胞移植产生了对神经元丢失的整体预防,并且 CDK5 敲低星形胶质细胞显著增加了血管周围分支中内源性 GFAP 的免疫反应性(IR),同时在运动和体感区域血管壁中上调了 PECAM-1 IR,并增加了 SVZ 中的 Ki67 IR,部分与 BDNF 的产生有关。总之,我们的数据表明,shCDK5miR 星形胶质细胞的移植可保护缺血大鼠的神经血管单元,从而恢复运动和神经功能。