Suppr超能文献

衰老导致的室下区 Nrf2-ARE 通路破坏通过 PI3K-Wnt/β-连环蛋白失调导致帕金森病小鼠的神经发生损伤。

Aging-induced Nrf2-ARE pathway disruption in the subventricular zone drives neurogenic impairment in parkinsonian mice via PI3K-Wnt/β-catenin dysregulation.

机构信息

Oasi Maria Institute for Research and Care on Mental Retardation and Brain Aging, Neuropharmacology Section, 94018 Troina, Italy.

出版信息

J Neurosci. 2013 Jan 23;33(4):1462-85. doi: 10.1523/JNEUROSCI.3206-12.2013.

Abstract

Aging and exposure to environmental toxins including MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) are strong risk factors for developing Parkinson's disease (PD), a common neurologic disorder characterized by selective degeneration of midbrain dopaminergic (DAergic) neurons and astrogliosis. Aging and PD impair the subventricular zone (SVZ), one of the most important brain regions for adult neurogenesis. Because inflammation and oxidative stress are the hallmarks of aging and PD, we investigated the nature, timing, and signaling mechanisms contributing to aging-induced SVZ stem/neuroprogenitor cell (NPC) inhibition in aging male mice and attempted to determine to what extent manipulation of these pathways produces a functional response in the outcome of MPTP-induced DAergic toxicity. We herein reveal an imbalance of Nrf2-driven antioxidant/anti-inflammatory genes, such as Heme oxygenase1 in the SVZ niche, starting by middle age, amplified upon neurotoxin treatment and associated with an exacerbated proinflammatory SVZ microenvironment converging to dysregulate the Wingless-type MMTV integration site (Wnt)/β-catenin signaling, a key regulatory pathway for adult NPCs. In vitro experiments using coculture paradigms uncovered aged microglial proinflammatory mediators as critical inhibitors of NPC proliferative potential. We also found that interruption of PI3K (phosphatidylinositol3-kinase)/Akt and the Wnt/Fzd/β-catenin signaling cascades, which switch glycogen synthase kinase 3β (GSK-3β) activation on and off, were causally related to the impairment of SVZ-NPCs. Moreover, a synergy between dysfunctional microglia of aging mice and MPTP exposure further inhibited astrocyte proneurogenic properties, including the expression of key Wnts components. Last, pharmacological activation/antagonism studies in vivo and in vitro suggest the potential that aged SVZ manipulation is associated with DAergic functional recovery.

摘要

衰老和暴露于环境毒素,包括 MPTP(1-甲基-4-苯基-1,2,3,6-四氢吡啶),是导致帕金森病(PD)的强烈危险因素,PD 是一种常见的神经紊乱疾病,其特征是中脑多巴胺能(DAergic)神经元的选择性退化和星形胶质细胞增生。衰老和 PD 会损害侧脑室下区(SVZ),SVZ 是成年神经发生最重要的脑区之一。由于炎症和氧化应激是衰老和 PD 的标志,我们研究了导致衰老雄性小鼠 SVZ 干细胞/神经祖细胞(NPC)抑制的性质、时间和信号机制,并试图确定在多大程度上操纵这些途径会对 MPTP 诱导的 DAergic 毒性产生功能反应。我们在此揭示了 SVZ 生态位中 Nrf2 驱动的抗氧化/抗炎基因(如血红素加氧酶 1)的失衡,从中年开始,在神经毒素治疗时加剧,并与加剧的 SVZ 促炎微环境相关,导致 Wnt 型 MMV 整合位点(Wnt)/β-连环蛋白信号通路失调,这是成年 NPC 的关键调节途径。使用共培养范式的体外实验揭示了衰老的小胶质细胞促炎介质作为 NPC 增殖潜力的关键抑制剂。我们还发现,PI3K(磷脂酰肌醇 3-激酶)/Akt 和 Wnt/Fzd/β-连环蛋白信号级联的中断,这些信号级联开关糖原合酶激酶 3β(GSK-3β)的激活和失活,与 SVZ-NPC 的损伤有关。此外,衰老小鼠的功能失调小胶质细胞与 MPTP 暴露之间的协同作用进一步抑制了星形胶质细胞的神经发生特性,包括关键 Wnt 成分的表达。最后,体内和体外的药理学激活/拮抗研究表明,SVZ 老化的操纵与 DAergic 功能恢复有关。

相似文献

10
NT-020 treatment reduces inflammation and augments Nrf-2 and Wnt signaling in aged rats.
J Neuroinflammation. 2015 Sep 17;12:174. doi: 10.1186/s12974-015-0395-4.

引用本文的文献

2
The subventricular zone structure, function and implications for neurological disease.
Genes Dis. 2024 Aug 26;12(3):101398. doi: 10.1016/j.gendis.2024.101398. eCollection 2025 May.
3
Multi-omics analysis reveals the genetic aging landscape of Parkinson's disease.
Sci Rep. 2024 Dec 28;14(1):31167. doi: 10.1038/s41598-024-82470-z.
4
Wnt/β-catenin Signaling in Central Nervous System Regeneration.
Adv Exp Med Biol. 2025;1474:13-33. doi: 10.1007/5584_2024_830.
7
Role of Astrogliosis in the Pathogenesis of Parkinson's Disease: Insights into Astrocytic Nrf2 Pathway as a Potential Therapeutic Target.
CNS Neurol Disord Drug Targets. 2024;23(8):1015-1029. doi: 10.2174/0118715273270473231002104610.
8
Insight into Nrf2: a bibliometric and visual analysis from 2000 to 2022.
Front Genet. 2023 Sep 15;14:1266680. doi: 10.3389/fgene.2023.1266680. eCollection 2023.
9
10
An NRF2 Perspective on Stem Cells and Ageing.
Front Aging. 2021 Jun 15;2:690686. doi: 10.3389/fragi.2021.690686. eCollection 2021.

本文引用的文献

1
Wnt your brain be inflamed? Yes, it Wnt!
Trends Mol Med. 2013 Mar;19(3):144-56. doi: 10.1016/j.molmed.2012.12.001. Epub 2013 Jan 9.
2
LRRK2 functions as a Wnt signaling scaffold, bridging cytosolic proteins and membrane-localized LRP6.
Hum Mol Genet. 2012 Nov 15;21(22):4966-79. doi: 10.1093/hmg/dds342. Epub 2012 Aug 16.
3
Microglia modulate hippocampal neural precursor activity in response to exercise and aging.
J Neurosci. 2012 May 9;32(19):6435-43. doi: 10.1523/JNEUROSCI.5925-11.2012.
4
Effects of minocycline on endogenous neural stem cells after experimental stroke.
Neuroscience. 2012 Jul 26;215:174-83. doi: 10.1016/j.neuroscience.2012.04.036. Epub 2012 Apr 24.
5
Quantitative evaluation of the human subventricular zone.
Brain. 2012 Aug;135(Pt 8):e221, 1-4; author reply e222, 1-6. doi: 10.1093/brain/aws087. Epub 2012 Apr 25.
7
Impaired inflammatory responses in murine Lrrk2-knockdown brain microglia.
PLoS One. 2012;7(4):e34693. doi: 10.1371/journal.pone.0034693. Epub 2012 Apr 9.
8
Microglial activation - tuning and pruning adult neurogenesis.
Front Pharmacol. 2012 Mar 9;3:41. doi: 10.3389/fphar.2012.00041. eCollection 2012.
9
Minocycline-preconditioned neural stem cells enhance neuroprotection after ischemic stroke in rats.
J Neurosci. 2012 Mar 7;32(10):3462-73. doi: 10.1523/JNEUROSCI.5686-11.2012.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验