作者: R. D. Spence , M. E. Hamby , E. Umeda , N. Itoh , S. Du
关键词:
摘要: Estrogen has well-documented neuroprotective effects in a variety of clinical and experimental disorders the CNS, including autoimmune inflammation, traumatic injury, stroke, neurodegenerative diseases. The beneficial estrogens CNS include mitigation symptoms, as well attenuation histopathological signs neurodegeneration inflammation. cellular mechanisms that underlie these are uncertain, because number different cell types express estrogen receptors peripheral immune system CNS. Here, we investigated potential roles two endogenous estrogen-mediated neuroprotection. We selectively deleted receptor-α (ERα) from either neurons or astrocytes using well-characterized Cre-loxP systems for conditional gene knockout mice, studied deletions on ERα ligand-mediated model adoptive encephalomyelitis (EAE). found pronounced significant systemic treatment with ligand function, axonal loss during EAE were completely prevented by deletion astrocytes, whereas had no effect. These findings show signaling through but not neurons, is essential EAE. Our reveal unique mechanism have implications understanding pathophysiology sex hormone diverse disorders.