ArticleMolecular and cellular biochemistry2017
The role of actin depolymerizing factor in advanced glycation endproducts-induced impairment in mouse brain microvascular endothelial cells.
Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 6 citations in OpenAlex.
- The role of ROCK1/MLC/NMMHC IIA-actin signaling in ischemic stroke-induced blood-brain barrier disruption: implications for therapeutic intervention.Cellular and molecular life sciences : CMLS · 2025Article
- Tetramethylpyrazine ameliorates LPS-induced acute lung injury via the miR-369-3p/DSTN axis.Scientific reports · 2024Article
- Article
- The Role of RASGRP2 in Vascular Endothelial Cells-A Mini Review.International journal of molecular sciences · 2021Review
- RasGRP2 inhibits glyceraldehyde-derived toxic advanced glycation end-products from inducing permeability in vascular endothelial cells.Scientific reports · 2021Article
- Advanced glycation end-products disrupt brain microvascular endothelial cell barrier: The role of mitochondria and oxidative stress.Microvascular research · 2021Article
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 1 institution in 1 country.
Funding
Abstract
Endothelial dysfunction is one of the most important pathological events during the development of several diabetic complications including stroke. The aim of this work was to investigate the role of actin depolymerizing factor (ADF) in advanced glycation endproducts (AGEs)-induced impairment in mouse brain microvascular endothelial cells (MBMECs). Incubation of MBMECs with AGEs led to downregulation of expression of ADF, which was reversed by treatment with soluble receptor of AGEs or tempol (an antioxidant). Incubation of MBMECs with AGEs enhanced ratio of F/G-actin, increased endothelial permeability and reduced vasculogenic property, which was attenuated by overexpression of ADF. Furthermore, overexpression of ADF attenuated AGEs-induced downregulation of zonula occludens-1 and dephosphorylation of vascular endothelial growth factor receptor 2. Incubation of MBMECs with AGEs downregulated dimethylarginine dimethylaminohydrolase 2, enhanced formation of asymmetric dimethylarginine and reduced formation of nitric oxide, which was attenuated by overexpression of ADF. Incubation of MBMECs with AGEs induced activation of NF-κB, upregulated RAGE and enhanced formation of reactive oxygen species, which was attenuated by overexpression of ADF. Additionally, knockdown of ADF aggravated AGEs-induced impairment in endothelial permeability and vasculogenic property in MBMECs. In conclusion, AGEs treatment increased endothelial permeability and reduced vasculogenic property of MBMECs, at least in part, via downregulation of ADF.
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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.