ArticleAging cell2015
MARCKS-dependent mucin clearance and lipid metabolism in ependymal cells are required for maintenance of forebrain homeostasis during aging.
Article in Aging cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Age‑dependent and post‑intraventricular hemorrhage remodeling of the ependymal glycocalyx in mice.Fluids and barriers of the CNS · 2025Article
- IGFBP-2 and IGF-II: Key Components of the Neural Stem Cell Niche? Implications for Glioblastoma Pathogenesis.International journal of molecular sciences · 2025Review
- The translational landscape of reactive astrocytes reveals the impact of eIF2B-mediated dysregulation in VWM disease.NAR molecular medicine · 2025Article
- Marcks overexpression in retinal ganglion cells promotes optic nerve regeneration.Cell death & disease · 2024Article
- Multiciliated ependymal cells: an update on biology and pathology in the adult brain.Acta neuropathologica · 2024Review
- Ependyma in Neurodegenerative Diseases, Radiation-Induced Brain Injury and as a Therapeutic Target for Neurotrophic Factors.Biomolecules · 2023Review
- Roles of Ependymal Cells in the Physiology and Pathology of the Central Nervous System.Aging and disease · 2023Review
- Phosphorylation-dependent proteome of Marcks in ependyma during aging and behavioral homeostasis in the mouse forebrain.GeroScience · 2022Article
- Glioblastoma disrupts the ependymal wall and extracellular matrix structures of the subventricular zone.Fluids and barriers of the CNS · 2022Article
- Ependymal cells and neurodegenerative disease: outcomes of compromised ependymal barrier function.Brain communications · 2022Review
- IIIG9 inhibition in adult ependymal cells changes adherens junctions structure and induces cellular detachment.Scientific reports · 2021Article
- The adult human subventricular zone: partial ependymal coverage and proliferative capacity of cerebrospinal fluid.Brain communications · 2020Article
- Marcksb plays a key role in the secretory pathway of zebrafish Bmp2b.PLoS genetics · 2019Article
- MARCKS Is Necessary for Netrin-DCC Signaling and Corpus Callosum Formation.Molecular neurobiology · 2018Article
- MARCKS regulates neuritogenesis and interacts with a CDC42 signaling network.Scientific reports · 2018Article
- MARCKS and MARCKS-like proteins in development and regeneration.Journal of biomedical science · 2018Review
- Foxj1 expressing ependymal cells do not contribute new cells to sites of injury or stroke in the mouse forebrain.Scientific reports · 2018Article
- Cattle encephalon glycoside and ignotin reduced white matter injury and prevented post-hemorrhagic hydrocephalus in a rat model of intracerebral hemorrhage.Scientific reports · 2016Article
- Investigating the role of filamin C in Belgian patients with frontotemporal dementia linked to GRN deficiency in FTLD-TDP brains.Acta neuropathologica communications · 2015Article
- X MARCKS the spot: myristoylated alanine-rich C kinase substrate in neuronal function and disease.Frontiers in cellular neuroscience · 2015Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Ependymal cells (ECs) form a barrier responsible for selective movement of fluids and molecules between the cerebrospinal fluid and the central nervous system. Here, we demonstrate that metabolic and barrier functions in ECs decline significantly during aging in mice. The longevity of these functions in part requires the expression of the myristoylated alanine-rich protein kinase C substrate (MARCKS). Both the expression levels and subcellular localization of MARCKS in ECs are markedly transformed during aging. Conditional deletion of MARCKS in ECs induces intracellular accumulation of mucins, elevated oxidative stress, and lipid droplet buildup. These alterations are concomitant with precocious disruption of ependymal barrier function, which results in the elevation of reactive astrocytes, microglia, and macrophages in the interstitial brain tissue of young mutant mice. Interestingly, similar alterations are observed during normal aging in ECs and the forebrain interstitium. Our findings constitute a conceptually new paradigm in the potential role of ECs in the initiation of various conditions and diseases in the aging brain.
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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.