ArticleCell death & disease2017
MicroRNA-195 prevents dendritic degeneration and neuron death in rats following chronic brain hypoperfusion.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 60 citations in OpenAlex.
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- Protein swarm-based cause-effect analysis: effects of microRNAs on cooperation networks linking COVID-19 infections, atherosclerosis, and Alzheimer's disease.Frontiers in cardiovascular medicine · 2025Article
- G-CSF improved the memory and dendritic morphology impairments in the hippocampal CA1 pyramidal neurons after brain ischemia in the male rats.Metabolic brain disease · 2023Article
- Combination Therapy with Platelet-Rich Plasma and Epidermal Neural Crest Stem Cells Increases Treatment Efficacy in Vascular Dementia.Stem cells international · 2023Article
- MicroRNAs in Learning and Memory and Their Impact on Alzheimer's Disease.Biomedicines · 2022Review
- Genetic Deficiency of MicroRNA-15a/16-1 Confers Resistance to Neuropathological Damage and Cognitive Dysfunction in Experimental Vascular Cognitive Impairment and Dementia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Structural Plasticity of the Hippocampus in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- RNA sequencing-based identification of the regulatory mechanism of microRNAs, transcription factors, and corresponding target genes involved in vascular dementia.Frontiers in neuroscience · 2022Article
- Plasma microRNA vary in association with the progression of Alzheimer's disease.Alzheimer's & dementia (Amsterdam, Netherlands) · 2022Article
- The promise of microRNA-based therapies in Alzheimer's disease: challenges and perspectives.Molecular neurodegeneration · 2021Review
- The Potential Role of miRNAs as Predictive Biomarkers in Neurodevelopmental Disorders.Journal of molecular neuroscience : MN · 2021Review
- AhR/miR-23a-3p/PKCα axis contributes to memory deficits in ovariectomized and normal aging female mice.Molecular therapy. Nucleic acids · 2021Article
- An Insight into the microRNAs Associated with Arteriovenous and Cavernous Malformations of the Brain.Cells · 2021Review
- Lentivirus-Carried microRNA-195 Rescues Memory Deficits of Alzheimer's Disease Transgenic Mouse by Attenuating the Generation of Amyloid Plaques.Frontiers in pharmacology · 2021Article
- Regulatory microRNAs and vascular cognitive impairment and dementia.CNS neuroscience & therapeutics · 2020Review
- MicroRNA-195 prevents hippocampal microglial/macrophage polarization towards the M1 phenotype induced by chronic brain hypoperfusion through regulating CX3CL1/CX3CR1 signaling.Journal of neuroinflammation · 2020Article
- Metoprolol prevents neuronal dendrite remodeling in a canine model of chronic obstructive sleep apnea.Acta pharmacologica Sinica · 2020Article
- microRNA-195 attenuates neuronal apoptosis in rats with ischemic stroke through inhibiting KLF5-mediated activation of the JNK signaling pathway.Molecular medicine (Cambridge, Mass.) · 2020Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impaired synaptic plasticity and neuron loss are hallmarks of Alzheimer's disease and vascular dementia. Here, we found that chronic brain hypoperfusion (CBH) by bilateral common carotid artery occlusion (2VO) decreased the total length, numbers and crossings of dendrites and caused neuron death in rat hippocampi and cortices. It also led to increase in N-terminal β-amyloid precursor protein (N-APP) and death receptor-6 (DR6) protein levels and in the activation of caspase-3 and caspase-6. Further study showed that DR6 protein was downregulated by miR-195 overexpression, upregulated by miR-195 inhibition, and unchanged by binding-site mutation and miR-masks. Knockdown of endogenous miR-195 by lentiviral vector-mediated overexpression of its antisense molecule (lenti-pre-AMO-miR-195) decreased the total length, numbers and crossings of dendrites and neuron death, upregulated N-APP and DR6 levels, and elevated cleaved caspase-3 and caspase-6 levels. Overexpression of miR-195 using lenti-pre-miR-195 prevented these changes triggered by 2VO. We conclude that miR-195 is involved in CBH-induced dendritic degeneration and neuron death through activation of the N-APP/DR6/caspase pathway.
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