MicroRNA-210-5p Contributes to Cognitive Impairment in Early Vascular Dementia Rat Model Through Targeting Snap25

Ren, Zhenxing; Yu, Junlong; Wu, Zimei; Si, Wenwen; Li, Xianqian; Liu, Yuqing; Deng, Ran; Chen, Dong Feng

doi:10.3389/fnmol.2018.00388

Cited by 48 publications

(35 citation statements)

References 64 publications

(64 reference statements)

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“…Vascular dementia (VD) is the second common type of dementia (Ragusa et al, 2016;Ren et al, 2018 (Ren et al, 2018).…”

Section: Vascular Dementiamentioning

confidence: 99%

“…Vascular dementia (VD) is the second common type of dementia (Ragusa et al, 2016; Ren et al, 2018). Decreased cerebral blood flow and damaged blood vessels trigger VD, initially characterized by learning and memory impairment.…”

Section: Neurological Disorders Associated With Cognitive Impairmentmentioning

confidence: 99%

“…It is well understood that miR‐210‐5p is causative of synaptic deficit in chronic cerebral ischemia‐induced VD while downregulating synaptosome‐associated protein 25 (Snap25) and further harming cognitive function. Moreover, miR‐210‐5p agomir expands the latency during MWM testing (as an index of learning) with VD through synaptic pruning, indicating worsened memory (Ren et al, 2018).…”

Section: Neurological Disorders Associated With Cognitive Impairmentmentioning

confidence: 99%

See 2 more Smart Citations

MicroRNA alterations in neuropathologic cognitive disorders with an emphasis on dementia: Lessons from animal models

Bahlakeh

Gorji

Soltani

et al. 2020

Journal Cellular Physiology

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Cognitive dysfunction is a state of losing or having difficulties in remembering, learning, focusing, or making decisions that impact individual healthy life. Small single-stranded and nonprotein coding RNAs, microRNAs (miRNAs) participate actively in regulatory processes, incorporate cognitive signaling pathways, and intensely affect cognitive evolution. miRNAs exert their modification activities through translational or transcriptional processes. Reportedly, cognitive impairment and dementia are rising, especially in developing countries. Herein we provided a brief review of original studies addressing miRNA changes in the most common neurological diseases with a focus on dementia and Alzheimer's disease. It must be How to cite this article: Bahlakeh G, Gorji A, Soltani H, Ghadiri T. MicroRNA alterations in neuropathologic cognitive disorders with an emphasis on dementia: Lessons from animal models.

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“…Vascular dementia (VD) is the second common type of dementia (Ragusa et al, 2016;Ren et al, 2018 (Ren et al, 2018).…”

Section: Vascular Dementiamentioning

confidence: 99%

Section: Neurological Disorders Associated With Cognitive Impairmentmentioning

confidence: 99%

Section: Neurological Disorders Associated With Cognitive Impairmentmentioning

confidence: 99%

See 1 more Smart Citation

MicroRNA alterations in neuropathologic cognitive disorders with an emphasis on dementia: Lessons from animal models

Bahlakeh

Gorji

Soltani

et al. 2020

Journal Cellular Physiology

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“…Research investigating temporal-lobe epilepsy in rodent models has also identified differential miR-210 expression, predominantly overexpression in hippocampal regions in both chronic and acute epilepsy stages at time points ranging from 3 hours to 4 months following seizure induction (Gorter et al, 2014;Kretschmann et al, 2015;Schouten et al, 2015). Another rodent study has also highlighted that in rats subjected to 4 weeks of ischemia, modulation of the more divergent miR-210-5p guide strand affected synaptic density in the hippocampus and spatial memory performance in the Morris water maze (Ren et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-210 Knockout Alters Dendritic Density and Behavioural Flexibility

Watts

Williams

Lü

et al. 2019

Preprint

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MicroRNAs exert post-transcriptional control over eukaryotic genomes and are integral for regulating complex functions in neurodevelopment, neuroplasticity and cognitive processing. The microRNA-210 (miR-210) is a highly-conserved, hypoxia-regulated miRNA that has been shown to be dysregulated in Alzheimer's Disease. We have recently also identified a significant enrichment of neurodegenerative diseases among miR-210 targets within the human transcriptome. To further elucidate the role of miR-210 in neuronal function and cognitive behaviour, we utilised conditional miR-210 knockout mice to characterise miR-210 regulation and function in primary hippocampal neurons and measured visual discrimination and reversal learning using rodent touchscreen assays.We found that miR-210 expression was induced by neuronal activation and loss of neuronal miR-210 increased oxidative metabolism and ROS production as well as dendritic density and branching in vitro. We also found that loss of miR-210 in knockout mice increased behavioural flexibility and reduced perseverative responding during reversal learning which required updating of information and feedback. These data support a conserved, activity-dependent role for miR-210 in cognitive function through modulation of neuronal metabolism.

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“…miR-210 has two versions, miR-210-3P and miR-210-5P. miR-210-3p is the guide-strand that integrates into the RISC (RNA induced silencing complex), whereas miR-210-5p is the passenger-strand that is inactivated through degradation [19,20]. miR-210-5P is up-regulated in several malignant tumors that are associated with a variety of functionally important targets involved in cancer [21].…”

Section: Introductionmentioning

confidence: 99%

Mitophagy Promotes Sorafenib Resistance through Hypoxia-Inducible ATAD3A Dependent Axis

Wang

Liu

et al. 2020

Preprint

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Background: The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients. Methods: Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O 2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir. Results: We found a hyperactivated mitophagy regulating by ATAD3A-PINK/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice. Conclusions: Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC. Keywords: Mitophagy, ATAD3A, Hypoxia, Sorafenib resistance

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MicroRNA-210-5p Contributes to Cognitive Impairment in Early Vascular Dementia Rat Model Through Targeting Snap25

Cited by 48 publications

References 64 publications

MicroRNA alterations in neuropathologic cognitive disorders with an emphasis on dementia: Lessons from animal models

MicroRNA alterations in neuropathologic cognitive disorders with an emphasis on dementia: Lessons from animal models

MicroRNA-210 Knockout Alters Dendritic Density and Behavioural Flexibility

Mitophagy Promotes Sorafenib Resistance through Hypoxia-Inducible ATAD3A Dependent Axis

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