Steliga Aleksandra, Lietzau Grazyna, Wójcik Sławomir, Kowiański Przemysław
Institute of Health Sciences, Pomeranian University in Słupsk, Bohaterów Westerplatte 64, 76-200 Słupsk, Poland.
Division of Anatomy and Neurobiology, Faculty of Medicine, Medical University of Gdańsk, Dębinki 1, 80-211 Gdańsk, Poland.
J Chem Neuroanat. 2023 Jan;127:102192. doi: 10.1016/j.jchemneu.2022.102192. Epub 2022 Nov 17.
Brain injury triggers a complex response involving morphological changes, cellular proliferation, and differentiation of newly formed neuroglial subpopulations. These processes have been extensively studied in animal stroke models with permanent large vessel occlusion. However, less is known about neuroglial response after transient cerebral ischemia. Herein, we aimed to determine an astrocytic and NG2 glial proliferative response, potential changes in expression of developmental neuroglial markers: vimentin, nestin, oligodendrocyte transcription marker (Olig2), and a role of neuroglial subpopulations as a source of cells replenishing structural deficiencies in the ischemic brain. Results showed an induction of a proliferative neuroglial response in the peri-infarct area reflected in an increased percentage of GFAP/Ki67 + and NG2/Ki67 + cells within 4 weeks after transient MCAO. The peak of GFAP+ astrocytes proliferation of 30.3 ± 10.3% was observed in the first week, and a peak of NG2 + cells proliferation of 23.1 ± 11.8% in the second week after stroke. The presence of GFAP/Vimentin+ and GFAP/Nestin+ cells, as well as GFAP/Olig2 + and NG2/Olig2 + cells indicated an induction of developmental phenotypes with a differentiation potential. Finally, observed between day 1 and week 3 transient GFAP/NG2 + colocalization suggests the heterogeneous source of the reactive neuroglia after transient MCAO. Altogether, one-hour MCAO is a sufficient pathological stimulus to trigger a strong proliferative response of GFAP+ and NG2 + neuroglial cells and induce their early developmental phenotype. Our results suggest that transient ischemia may initiate a change in the direction of differentiation within the neuroglia cell population.
脑损伤引发了一种复杂的反应，涉及形态学变化、细胞增殖以及新形成的神经胶质亚群的分化。这些过程在永久性大血管闭塞的动物中风模型中已得到广泛研究。然而，关于短暂性脑缺血后的神经胶质反应，我们了解得较少。在此，我们旨在确定星形胶质细胞和NG2胶质细胞的增殖反应、发育性神经胶质标志物波形蛋白、巢蛋白、少突胶质细胞转录标志物（Olig2）表达的潜在变化，以及神经胶质亚群作为补充缺血性脑结构缺陷的细胞来源的作用。结果显示，在短暂性大脑中动脉闭塞（MCAO）后4周内，梗死周围区域诱导了增殖性神经胶质反应，表现为GFAP/Ki67 +和NG2/Ki67 +细胞百分比增加。在中风后的第一周观察到GFAP +星形胶质细胞增殖峰值为30.3±10.3%，第二周观察到NG2 +细胞增殖峰值为23.1±11.8%。GFAP/波形蛋白 +和GFAP/巢蛋白 +细胞，以及GFAP/Olig2 +和NG2/Olig2 +细胞的存在表明诱导了具有分化潜能的发育表型。最后，在第1天至第3周观察到的短暂性GFAP/NG2 +共定位表明短暂性MCAO后反应性神经胶质的异质性来源。总之，1小时的MCAO是触发GFAP +和NG2 +神经胶质细胞强烈增殖反应并诱导其早期发育表型的充分病理刺激。我们的结果表明，短暂性缺血可能引发神经胶质细胞群体分化方向的改变。
