Lev Nirit, Barhum Yael, Melamed Eldad, Offen Daniel
Felsenstein Medical Research Center, Beilinson Campus, Tel Aviv University, Sackler School of Medicine, Petah-Tikva, Israel.
Neurosci Lett. 2004 Apr 15;359(3):139-42. doi: 10.1016/j.neulet.2004.01.076.
Multiple sclerosis (MS) is an inflammatory disease of the central nervous system characterized by demyelination and axonal damage. Although the exact pathophysiology is unknown, apoptosis plays a crucial role. Here, we studied the role of the pro-apoptotic gene Bax in myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE), the animal model for MS. We demonstrate that the clinical signs were markedly reduced in the EAE Bax-deficient mice as compared to wild type (2.3 +/- 0.5 vs. 1.02 +/- 0.32, respectively, P < 0.05). Bax-deficient mice demonstrated less inflammatory infiltration and axonal damage, although they showed similar T-cell immune potency. In conclusion, ablation of the bax gene attenuates the severity of MOG-induced EAE and emphasizes the importance of apoptosis in the pathogenesis of EAE and MS.
多发性硬化症（MS）是一种中枢神经系统的炎症性疾病，其特征为脱髓鞘和轴突损伤。尽管确切的病理生理学尚不清楚，但细胞凋亡起着关键作用。在此，我们研究了促凋亡基因Bax在髓鞘少突胶质细胞糖蛋白（MOG）诱导的实验性自身免疫性脑脊髓炎（EAE）中的作用，EAE是MS的动物模型。我们证明，与野生型相比，EAE Bax缺陷小鼠的临床症状明显减轻（分别为2.3±0.5和1.02±0.32，P<0.05）。Bax缺陷小鼠表现出较少的炎症浸润和轴突损伤，尽管它们显示出相似的T细胞免疫效力。总之，bax基因的缺失减轻了MOG诱导的EAE的严重程度，并强调了细胞凋亡在EAE和MS发病机制中的重要性。
