ANTI-AMYLOIDOGENIC EFFECT OF MiR-101 IN EXPERIMENTAL ALZHEIMER’S DISEASE

Sokolik, V. V.

doi:10.15407/biotech12.03.041

Cited by 5 publications

(3 citation statements)

References 45 publications

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“…It is for this reason that miRNAs have attracted extensive attention as predictive and diagnostic biomarkers for the occurrence and progression of AD [ 10 ]. Nowadays, a large number of miRNAs including miR-101 [ 11 ], miR-107 [ 12 ], miR-29 [ 13 ], and miR-124 [ 14 ] are regarded as promising diagnostic biomarkers for AD. Specifically, miR-590-5p is shown to be expressed at lower levels in serum of AD patients than that in healthy subjects based on GSE147232 from GEO database.…”

Section: Introductionmentioning

confidence: 99%

miR-590-5p Overexpression Alleviates β-Amyloid-Induced Neuron Damage via Targeting Pellino-1

Lin

Peng

Chen

et al. 2022

Analytical Cellular Pathology

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Alzheimer’s disease (AD) is one common degenerative disorder. However, the effects of miR-590-5p on AD and the mechanism on modulation of AD development were unclear. In this study, the miR-590-5p level in AD patients at mild, moderate, and severe stage as well as APP/PS1 transgenic mice was detected by qRT-PCR. The relationship of miR-590-5p and pellino-1 (PELI1) was identified by double luciferase reporter gene assay. Afterwards, both BV-2 and HT22 cells were exposed to β-amyloid (Aβ) peptides to mimic AD cell model. Then, the roles of miR-590-5p upregulation or PELI1 silence in cell proliferation and apoptosis were explored by CCK-8 assay and TUNEL assay, and the expression of apoptosis-related proteins was detected by western blotting. Furthermore, the involvements of the downstream Traf3/MAPK P38 pathway with the roles of miR-590-5p in AD were measured by western blotting. Our results showed that knockdown of miR-590-5p was found in AD patients, mice model, and Aβ-induced cell model. Notably, PELI1 was proved as a target gene of miR-590-5p. miR-590-5p mimic or PELI1 silence significantly promoted cell proliferation and inhibited cell apoptosis, as well as suppressed the activation of Traf3/MAPK P38 pathway both in Aβ-induced BV-2 and HT22 cells. The effects of PELI1 overexpression on cell proliferation, apoptosis, and Traf3/MAPK P38 pathway were partly abrogated by miR-590-5p mimic both in BV-2 and HT22 cells. In conclusion, miR-590-5p was expressed at lower levels in AD, and miR-590-5p/PELI1 axis might be involved in the progression of AD by the downstream Traf3/MAPK P38 pathway.

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Section: Introductionmentioning

confidence: 99%

miR-590-5p Overexpression Alleviates β-Amyloid-Induced Neuron Damage via Targeting Pellino-1

Lin

Peng

Chen

et al. 2022

Analytical Cellular Pathology

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“…Changes in working, spatial and emotional memory in rats caused by intrahypocampal administration of β-amyloid peptide 40 aggregates, are associated with impaired storage and retrieval of information about the experience due to dysfunction of brain structures -hippocampus and anterior neocortex, which agrees with the data (Mugantseva & Podolski, 2009) on the weakening of the interneuronal connections between the hippocampus and the neocortex under the action of aggregated β-amyloid peptide. Earlier Sokolik et al (2019) showed that the introduction of Aβ40 aggregates into the hippocampus leads to an increase in the concentration of toxic endogenous Aβ42 by 36.2% in the neocortex and 27.3% in the hippocampus. This increase in the concentration of toxic β-amyloid peptide 42 is characteristic of the development of preclinical and early clinical stages of Alzheimer's disease, when the clinical manifestations of the disease are compensated by brain mechanisms (Purdenko, 2014).…”

Section: Discussionmentioning

confidence: 99%

The effect of miR-101 on the memory of rats with a model of Alzheimer’s disease

Берченко

Levicheva

Bevzyuk

et al. 2020

Regul. Mech. Biosyst.

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Memory impairment is a hallmark of Alzheimer’s disease. The clinical diagnosis of the disease is made in the later stages of its development, when specific therapy of the disease is not always effective. Therefore, the detection of early behavioral manifestations of memory disorders in the development of the disease will allow the use of preventive therapy aimed at stopping the death of neurons in brain structures. A neuroethological study of working, spatial, and emotional memory was performed in rats 15–16 months of age with a model of early manifestations of Alzheimer’s disease induced by stereotactic administration of β-amyloid peptide 40 aggregates into the hippocampus. Changes in the neuroethological components of working and spatial memory have been identified. Testing of working memory showed a violation in rats of recognizing the shape of identical objects, reducing experimental activity to unfamiliar objects and their differentiation. Spatial orientation disorders have been identified in the Barnes labyrinth. Emotional memory research has shown the preservation of innate forms of protective adaptive behaviour. At the same time, vegetative indicators reflected an increase in emotional tension. Intranasal administration of liposomal miRNA miR-101 involved in liposomes to rats with a model of early manifestations of Alzheimer’s disease improved neuroethological parameters of working and spatial memory. Restoration of the level of research activity and differentiation of familiar and unfamiliar objects in the testing of working memory in rats has been established. Spatial memory in Barnes labyrinth testing was improved by reproducing spatial orientation skills and relieving emotional stress. Thus, the intranasal use of miR-101 in Alzheimer’s disease is a promising approach to prevent the development of amyloidosis and preserve memory in the early manifestations of Alz-heimer’s disease.

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“…In our previous studies, the predominantly anti-amyloidogenic and/or anti-inflammatory effects of liposomal preparations of CUR and miR-101 have been established individually in animal and cellular models of Alzheimer's disease Shulga, 2015, 2016;Sokolik et al, 2017Sokolik et al, , 2019Sokolik et al, , 2021. Therefore, it is logical that the aim of this study was to study the effect of miR-101 + CUR in a single liposome in an experimental AD model in vitro.…”

Section: Introductionmentioning

confidence: 97%

The cumulative effect of the combined action of miR-101 and curcumin in a liposome on a model of Alzheimer’s disease in mononuclear cells

Sokolik

Берченко

2023

Front. Cell. Neurosci.

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The leading pathological mechanisms of Alzheimer’s disease (AD) are amyloidosis and chronic inflammation. The study of new therapeutic drugs of the corresponding action, in particular miRNAs and curcominoids, as well as methods for their packaging, is topical. The aim of the work was to study the effect of miR-101 + curcumin in a single liposome in a cellular AD model. AD model was made by incubating a suspension of mononuclear cells with aggregates of beta-amyloid peptide 1–40 (Aβ40) for 1 h. The effect of the subsequent application of liposomal (L) preparations miR-101, curcumin (CUR), and miR-101 + CUR was analyzed over time of 1, 3, 6, and 12 h. A decrease in the level of endogenous Aβ42 under the influence of L(miR-101 + CUR) was revealed during the entire incubation period (1–12 h), the first part of which was overlapped due to inhibition of mRNAAPP translation by miR-101 (1–3 h), and the second-by inhibition of mRNAAPP transcription by curcumin (3–12 h), the minimum concentration of Aβ42 was recorded at 6 h. The cumulative effect of the combination drug L(miR-101 + CUR) was manifested in the suppression of the increase in the concentration of TNFα and IL-10 and a decrease in the concentration of IL-6 during the entire incubation period (1–12 h). Thus, miR-101 + CUR in one liposome enhanced each other’s antiamyloidogenic and anti- inflammatory effects in a cellular AD model.

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ANTI-AMYLOIDOGENIC EFFECT OF MiR-101 IN EXPERIMENTAL ALZHEIMER’S DISEASE

Cited by 5 publications

References 45 publications

miR-590-5p Overexpression Alleviates β-Amyloid-Induced Neuron Damage via Targeting Pellino-1

miR-590-5p Overexpression Alleviates β-Amyloid-Induced Neuron Damage via Targeting Pellino-1

The effect of miR-101 on the memory of rats with a model of Alzheimer’s disease

The cumulative effect of the combined action of miR-101 and curcumin in a liposome on a model of Alzheimer’s disease in mononuclear cells

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