ArticleBrain research2012
AP-2β regulates amyloid beta-protein stimulation of apolipoprotein E transcription in astrocytes.
Article in Brain research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Amyloid Precursor Protein and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- The regulatory role of AP-2β in monoaminergic neurotransmitter systems: insights on its signalling pathway, linked disorders and theragnostic potential.Cell & bioscience · 2022Review
- Astrocytic Calcium and cAMP in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- Tocotrienol Rich Fraction Supplementation Modulate Brain Hippocampal Gene Expression in APPswe/PS1dE9 Alzheimer's Disease Mouse Model.Journal of Alzheimer's disease : JAD · 2019Article
- High-density lipoprotein mimetic peptide 4F mitigates amyloid-β-induced inhibition of apolipoprotein E secretion and lipidation in primary astrocytes and microglia.Journal of neurochemistry · 2018Article
- RXR controlled regulatory networks identified in mouse brain counteract deleterious effects of Aβ oligomers.Scientific reports · 2016Article
- Molecular approaches for manipulating astrocytic signaling in vivo.Frontiers in cellular neuroscience · 2015Review
- Neuroinflammation in Alzheimer's disease.Neuropsychiatric disease and treatment · 2015Review
- Cholesterol as a causative factor in Alzheimer's disease: a debatable hypothesis.Journal of neurochemistry · 2014Review
- Mechanisms of U87 astrocytoma cell uptake and trafficking of monomeric versus protofibril Alzheimer's disease amyloid-β proteins.PloS one · 2014Article
- Inhibition of APE1/Ref-1 redox activity rescues human retinal pigment epithelial cells from oxidative stress and reduces choroidal neovascularization.Redox biology · 2014Article
- Transcriptional regulation and its misregulation in Alzheimer's disease.Molecular brain · 2013Review
- Amyloid β inhibits retinoic acid synthesis exacerbating Alzheimer disease pathology which can be attenuated by an retinoic acid receptor α agonist.The European journal of neuroscience · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Two key players involved in Alzheimer's disease (AD) are amyloid beta protein (Aβ) and apolipoprotein E (apoE). Aβ increases apoE protein levels in astrocytes which is associated with cholesterol trafficking, neuroinflammatory responses and Aβ clearance. The mechanism for the increase in apoE protein abundance is not understood. Based on different lines of evidence, we propose that the beta-adrenergic receptor (βAR), cAMP and the transcription factor activator protein-2 (AP-2) are contributors to the Aβ-induced increase in apoE abundance. This hypothesis was tested in mouse primary astrocytes and in cells transfected with an apoE promoter fragment with binding sites for AP-2. Aβ(42) induced a time-dependent increase in apoE mRNA and protein levels which were significantly inhibited by βAR antagonists. A novel finding was that Aβ incubation significantly reduced AP-2α levels and significantly increased AP-2β levels in the nuclear fraction. The impact of Aβ-induced translocation of AP-2 into the nucleus was demonstrated in cells expressing AP-2 and incubated with Aβ(42). AP-2 expressing cells had enhanced activation of the apoE promoter region containing AP-2 binding sites in contrast to AP-2 deficient cells. The transcriptional upregulation of apoE expression by Aβ(42) may be a neuroprotective response to Aβ-induced cytotoxicity, consistent with apoE's role in cytoprotection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.