ArticleAmerican journal of translational research2018
Control of macrophage autophagy by miR-384-5p in the development of diabetic encephalopathy.
Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Diabetes and brain: omics approaches to study diabetic encephalopathy.Frontiers in endocrinology · 2025Review
- Small RNA Sequencing Analysis of STZ-Injured Pancreas Reveals Novel MicroRNA and Transfer RNA-Derived RNA with Biomarker Potential for Diabetes Mellitus.International journal of molecular sciences · 2023Article
- Dysregulation of Serum MicroRNA after Intracerebral Hemorrhage in Aged Mice.Biomedicines · 2023Article
- Specific microRNAs for Modulation of Autophagy in Spinal Cord Injury.Brain sciences · 2022Review
- Virus, Exosome, and MicroRNA: New Insights into Autophagy.Advances in experimental medicine and biology · 2022Article
- Green tea protects against hippocampal neuronal apoptosis in diabetic encephalopathy by inhibiting JNK/MLCK signaling.Molecular medicine reports · 2021Article
- BMSC-Derived Exosomes Ameliorate LPS-Induced Acute Lung Injury by miR-384-5p-Controlled Alveolar Macrophage Autophagy.Oxidative medicine and cellular longevity · 2021Article
- Nicotinate-curcumin ameliorates cognitive impairment in diabetic rats by rescuing autophagic flux in CA1 hippocampus.CNS neuroscience & therapeutics · 2019Article
- Influence of hyperproteinemia on reproductive development in an invertebrate model.International journal of biological sciences · 2019Article
- miR-384-5p regulates inflammation inScience progressArticle
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular development of diabetic encephalopathy remains ill-defined. Recently, we reported that elimination of inflammatory macrophages alleviated the progress and severity of diabetic encephalopathy. Here, we studied the underlying mechanism. Inflammatory macrophages were isolated from the brain of the mice that received i.p. injection of streptozotocin (STZ) to develop diabetes 6 weeks before, and showed enhanced autophagy activity, seemingly through augmentation of Beclin-1 levels. However, the increases in Beclin-1 levels did not result from enhanced gene transcription, but appeared to result from suppression of a Beclin-1-inhibitory microRNA, miR-384-5p. Overexpression of miR-384-5p in the inflammatory macrophages through an adeno-associated virus mediated gene transfer system significantly reduced inflammatory macrophages in the diabetic brain, resulting in attenuation of the STZ-induced decreases in brain malondialdehyde, catalase and superoxidase anion-positive cells, and the STZ-induced increases in brain nitric oxide. Thus, these data suggest that downregulation of miR-384-5p in the inflammatory macrophages may enhance macrophage autophagy and contribute to the development of diabetic encephalopathy, which may be suppressed by re-expression of miR-384-5p in macrophages.
Indexed as
Identifiers
29511445PMC5835816W2977670482What OpenQuestion holds
Registered trials
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