ArticleAging2019
MeCP2 inhibits cell functionality through FoxO3a and autophagy in endothelial progenitor cells.
Article in Aging, 2019. 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, 24 citations in OpenAlex.
- The Nodding syndrome cerebrospinal fluid proteome: a lens into neurodevelopmental failure consistent with environmentally triggeredFrontiers in molecular neuroscience · 2026Article
- Characterization of Corneal Defects in ATG7-Deficient Mice.International journal of molecular sciences · 2025Article
- Dysregulation of autophagy during photoaging reduce oxidative stress and inflammatory damage caused by UV.Frontiers in pharmacology · 2025Review
- Downregulated SPESP1-driven fibroblast senescence decreases wound healing in aged mice.Clinical and translational medicine · 2024Article
- The role of autophagy in odontogenesis, dental implant surgery, periapical and periodontal diseases.Journal of cellular and molecular medicine · 2024Review
- Epigenetic regulation ofAutophagy · 2024Review
- Methylation across the central dogma in health and diseases: new therapeutic strategies.Signal transduction and targeted therapy · 2023Review
- Optogenetic engineered umbilical cord MSC-derived exosomes for remodeling of the immune microenvironment in diabetic wounds and the promotion of tissue repair.Journal of nanobiotechnology · 2023Article
- Autophagy-Modulated Biomaterial: A Robust Weapon for Modulating the Wound Environment to Promote Skin Wound Healing.International journal of nanomedicine · 2023Review
- Autophagy Plays Multiple Roles in the Soft-Tissue Healing and Osseointegration in Dental Implant Surgery-A Narrative Review.Materials (Basel, Switzerland) · 2022Review
- Role of autophagy and transcriptome regulation in acute brain injury.Experimental neurology · 2022Review
- Autophagy and skin wound healing.Burns & trauma · 2022Review
- Epigenetic Clock: DNA Methylation in Aging.Stem cells international · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesAutophagy is an evolutionarily conserved intracellular degradation mechanism in which cell constituents are phagocytosed to maintain cellular homeostasis. Forkhead box O 3a (FoxO3a) promotes autophagy to protect cells from environmental stress. Methylated CpG binding protein 2 (MeCP2) is a nuclear protein that binds DNA and represses transcription. However, the mechanism and interplay between FoxO3a and MeCP2 underlying endothelial progenitor cell (EPC) function are not fully understood.
resultsIn EPCs, MeCP2 overexpression attenuated autophagy and cell functionality, which were reversed by the autophagy activator rapamycin or co-transfection with FoxO3a. FoxO3a promoted cell function, which was reversed by the autophagy inhibitor chloroquine. Following MeCP2 overexpression, MeCP2 was found enriched on the FoxO3a promoter, resulting in promoter hypermethylation and enhanced H3K9 histone modification in nucleosomes of the FoxO3a promoter.
conclusionsMeCP2 attenuated cell functionality via DNA hypermethylation and histone modification of the FoxO3a promoter to inhibit FoxO3a transcription and autophagy. MATERIALS AND
methodsEPCs were isolated from human umbilical cord blood and treated with adenoviral vectors containing interference sequences. The effects and mechanism of MeCP2 and FoxO3a were analyzed by utilizing western blotting, cell counting kit-8, transwell plates, Matrigel, matrix adhesion, transmission electron microscopy, and chromatin immunoprecipitation.
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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.