ArticleAngiogenesis2024
The influences of ApoE isoforms on endothelial adherens junctions and actin cytoskeleton responding to mCRP.
Article in Angiogenesis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Peripheral vascular function, including endothelium-dependent measures, and dementia risk: The Framingham Heart Study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Circulating C-reactive protein influences polygenic risk of inflammatory genes expressed in brain endothelia for Alzheimer's disease.Neurobiology of disease · 2026Article
- Dynamic trajectories of inflammatory biomarkers and post-stroke cognitive impairment: a comprehensive review of neuroimmune mechanisms, longitudinal modeling, and clinical translation.Frontiers in neurology · 2026Review
- Monomeric C-reactive Protein Exacerbates Neuronal Injury and Enhances Microglial Activation after Global Cerebral Ischemia in Mice.Molecular neurobiology · 2025Article
- Review
- Association between the C-reactive protein-triglyceride-glucose index and endometriosis: a cross-sectional study using data from the national health and nutrition examination survey, 1996-2006.BMC women's health · 2025Article
- Redefining CRP in tissue injury and repair: more than an acute pro-inflammatory mediator.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Apolipoprotein E4 (ApoE4) plays an important role responding to monomeric C-reactive protein (mCRP) via binding to CD31 leading to cerebrovascular damage and Alzheimer's disease (AD). Using phosphor-proteomic profiling, we found altered cytoskeleton proteins in the microvasculature of AD brains, including increased levels of hyperphosphorylated tau (pTau) and the actin-related protein, LIMA1. To address the hypothesis that cytoskeletal changes serve as early pathological signatures linked with CD31 in brain endothelia in ApoE4 carriers, ApoE4 knock-in mice intraperitoneal injected with mCRP revealed that mCRP increased the expressions of phosphorylated CD31 (pCD31) and LIMA1, and facilitate the binding of pCD31 to LIMA1. mCRP combined with recombinant APOE4 protein decreased interaction of CD31 and VE-Cadherin at adherens junctions (AJs), along with altered the expression of various actin cytoskeleton proteins, causing microvasculature damage. Notably, the APOE2 protein attenuated these changes. Overall, our study demonstrates that ApoE4 responds to mCRP to disrupt the endothelial AJs which link with the actin cytoskeleton and this pathway could play a key role in the barrier dysfunction leading to AD risk.
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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.