Abstract
The aim of this study was to explore the specific role of miR-29c-3p in Alzheimer's disease (AD). Animal models of AD were established by injecting streptozotocin (STZ) into mice through the lateral ventricle, while cell models of AD were induced by 10 μM β-amyloid (Aβ). We detected miR-29c-3p and β-site amyloid precursor protein cleaving enzyme 1 (BACE1) contents and measured AD cell proliferation and apoptosis. A low miR-29c-3p level and a high BACE1 level were detected in the brain tissue of AD animal models and AD cell models. Aβ-processed cells had markedly lower proliferation activity, higher apoptosis, increased phosphorylation of tau protein was over phosphorylated, but the overexpression of miR-29c-3p or the silencing of BACE1 significantly enhanced the cell proliferation activity and reduced cell apoptosis by regulating the contents of related proteins. Inhibition of miR-29c-3p or overexpression of BACE1 aggravated Aβ-induced side effects. We used Targetscan7.2 to predict the downstream target genes of miR-29c-3p. Then, we detected that there were target binding sites between miR-29c-3p and BACE1. The rescue experiment identified BACE1 as a functional target for miR-29c-3p. AD leads to decreased miR-29c-3p level and increased BACE1 level. MiR-29c-3p has specific binding sites with the 3′-untranslated region (3′-UTR) of BACE1 and thus negatively regulates the BACE1 level, thereby affecting the progression of AD.
Highlights
Alzheimer’s disease (AD), a neurodegenerative disease common in old people, mainly manifests as impaired cognitive functions, social disorders, abnormal behaviors, and memory loss [1, 2]
One of the main pathological changes caused by AD is senile plaque deposition in the brain, which mainly consists of Aβ that comes from amyloid precursor protein Journal of Healthcare Engineering (APP) after being sequentially cleaved by c-secretase and β-site amyloid precursor protein cleaving enzyme 1 (BACE1), called β-secretase 1, a key gene for Aβ accumulation in the brain of AD patients [12, 13]
Mice in the control group were reared normally, while mice in the AD group were made into AD models by injecting streptozotocin (STZ) through the lateral ventricle [15]. is study was carried out after obtaining approval from the ethics committee of our hospital, in strict accordance with guidelines issued by the Care and Use of Laboratory Animal and the National Institutes of Health (NIH)
Summary
Alzheimer’s disease (AD), a neurodegenerative disease common in old people, mainly manifests as impaired cognitive functions, social disorders, abnormal behaviors, and memory loss [1, 2]. E occurrence of AD is related to β-amyloid (Aβ) plaques and neurofibrillary tangles (containing tau protein) in the cerebral cortex and subcortical regions, so there is the speculation that the reducing or eliminating of this substance from the brain may prevent or reverse the progression of AD disease [4, 5]. MiRNAs are highly expressed or expressed in the nervous system to affect neural development and synaptic functions and participate in processes such as memory formation and regulation of protein synthesis, as well as to induce specific neurodegenerative diseases [7,8,9]. MiR-29c-3p is abnormally expressed in a variety of diseases [10]. One of the main pathological changes caused by AD is senile plaque deposition in the brain, which mainly consists of Aβ that comes from amyloid precursor protein
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