Blood-Brain Barrier Group, Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA.
J Mol Neurosci. 2013 Mar;49(3):446-56. doi: 10.1007/s12031-012-9825-2. Epub 2012 Jun 10.
The detrimental role of leptin in experimental autoimmune encephalomyelitis (EAE) is opposite to its neuroprotective role in other neuropathologies. We hypothesize that a shifted cellular distribution of leptin receptors underlies the differential effects of leptin. A robust increase of ObR immunoreactivity was seen along glial fibrillary acidic protein (GFAP)(+) intermediate filaments in reactive astrocytes in the hippocampus and hypothalamus of mice with EAE. Although astrocyte-specific GFAP mRNA and protein were both increased, ObRa mRNA was elevated only after resolution of EAE symptoms, and ObRb mRNA was even decreased at the peak time of symptoms of EAE. A cell type-specific action of leptin may underlie its differential effects.
瘦素在实验性自身免疫性脑脊髓炎（EAE）中的有害作用与其在其他神经病理学中的神经保护作用相反。我们假设瘦素受体的细胞分布变化是导致瘦素产生不同作用的基础。在患有 EAE 的小鼠的海马体和下丘脑的反应性星形胶质细胞中，ObR 免疫反应性沿着神经胶质纤维酸性蛋白（GFAP）（+）中间丝显著增加。尽管星形胶质细胞特异性 GFAP mRNA 和蛋白均增加，但 ObRa mRNA 仅在 EAE 症状缓解后升高，而 ObRb mRNA 在 EAE 症状高峰期甚至降低。瘦素的细胞类型特异性作用可能是其产生不同作用的基础。
