The Role of Mineralocorticoid Receptor Expression in Brain Remodeling after Cerebral Ischemia

内科学 内分泌学 盐皮质激素受体 缺血 医学 神经保护 血管生成 血管内皮生长因子 碱性成纤维细胞生长因子 螺内酯 盐皮质激素 受体 生长因子 醛固酮 血管内皮生长因子受体
作者
Naofumi Oyamada,Masakatsu Sone,Kazutoshi Miyashita,Kwijun Park,Daisuke Taura,Megumi Inuzuka,Takuhiro Sonoyama,Hirokazu Tsujimoto,Yasutomo Fukunaga,Naohisa Tamura,Hiroshi Itoh,Kazuwa Nakao
出处
期刊:Endocrinology [Oxford University Press]
卷期号:149 (8): 3764-3777 被引量:54
标识
DOI:10.1210/en.2007-1770
摘要

Mineralocorticoid receptors (MRs) are classically known to be expressed in the distal collecting duct of the kidney. Recently it was reported that MR is identified in the heart and vasculature. Although MR expression is also found in the brain, it is restricted to the hippocampus and cerebral cortex under normal condition, and the role played by MRs in brain remodeling after cerebral ischemia remains unclear. In the present study, we used the mouse 20-min middle cerebral artery occlusion model to examine the time course of MR expression and activity in the ischemic brain. We found that MR-positive cells remarkably increased in the ischemic striatum, in which MR expression is not observed under normal conditions, during the acute and, especially, subacute phases after stroke and that the majority of MR-expressing cells were astrocytes that migrated to the ischemic core. Treatment with the MR antagonist spironolactone markedly suppressed superoxide production within the infarct area during this period. Quantitative real-time RT-PCR revealed that spironolactone stimulated the expression of neuroprotective or angiogenic factors, such as basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), whereas immunohistochemical analysis showed astrocytes to be cells expressing bFGF and VEGF. Thereby the incidence of apoptosis was reduced. The up-regulated bFGF and VEGF expression also appeared to promote endogenous angiogenesis and blood flow within the infarct area and to increase the number of neuroblasts migrating toward the ischemic striatum. By these beneficial effects, the infarct volume was significantly reduced in spironolactone-treated mice. Spironolactone may thus provide therapeutic neuroprotective effects in the ischemic brain after stroke.
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