MicroRNA-338-5p alleviates neuronal apoptosis via directly targeting BCL2L11 in APP/PS1 mice.
Open accessAbstract
MicroRNAs have become pivotal modulators in the pathogenesis of Alzheimer’s disease. MiR-338-5p is associated with neuronal differentiation and neurogenesis, and expressed aberrantly in patients with cognitive dysfunction. However, its role and potential mechanism involved in Alzheimer’s disease remain to be elucidated. Herein, we showed that the expression of miR-338-5p decreased in APP/PS1 mice, accompanied by the elevation in the expression level of amyloid β, which indicated a reverse relationship between Alzheimer’s disease progression and miR-338-5p. In addition, lentiviral overexpression of miR-338-5p through intrahippocampal injection mitigated the amyloid plaque deposition and cognitive dysfunction in APP/PS1 mice, suggesting a protecting role of miR-338-5p against the development of Alzheimer’s disease. Moreover, miR-338-5p decelerated apoptotic loss of neurons in APP/PS1 mice. MiR-338-5p decreased neuronal apoptosis in vitro induced by amyloid β accumulation, which was attributed to the negative regulation of BCL2L11 by miR-338-5p, since the restoration of BCL2L11 eliminated the protective role of miR-338-5p against neuronal apoptosis. Taken together, all of these results may indicate miR-338-5p as an innovative modulator in the pathogenesis of Alzheimer’s disease, and also suggest that the protective effect of miR-338-5p on neuronal apoptosis may underlie its beneficial effect on APP/PS1 mice.
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MiR-338-5p safeguards the cognitive function of transgenic APP/PS1 mice by lowering neuronal death.
“MiR-338-5p has been found to safeguard the cognitive function of transgenic APP/PS1 mice by lowering neuronal death [37].”
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“Among our predicted downstream factors, we have found that inhibition of Bcl2l11 and Ptgs2 can inhibit neuronal apoptosis (Xiao et al., 2019; Li et al., 2020) and that they are down-regulated in expression after nerve injury.”
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“In addition, overexpression of BCL2L11 eliminates the miR-338-5p protective role against apoptosis of neurons [45].”
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“Some studies have confirmed that caspase 3 is activated during Aβ-induced neuronal apoptosis (Chang et al., 2016) and that caspase 3 immunoreactivity is activated in patients with AD (Bredesen et al., 2006) and in animal models of AD (Li et al., 2020).”
Non-Coding RNAs and Neurodegenerative Diseases: Information of their Roles in Apoptosis
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Prophylactic Melatonin Treatment Ameliorated Propofol-Induced Cognitive Dysfunction in Aged Rats
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Regulation of Apoptotic Pathways by MicroRNAs: A Therapeutic Strategy for Alzheimer’s Disease
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“BCL2 like 11 (BCL2L11), also known as BIM, locates in the outer membrane of mitochondria and functions as a facilitator of mitochondrial apoptosis [34,35].”
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- Authors
- Li, J., Li, D., Zhou, H., Wu, G., He, Z., Liao, W., Li, Y., & Zhi, Y.
- Affiliations
- Sun Yat-sen University (CN)
- Corresponding author
- Li, Yujuan
- Zhi, Yaowei
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2020-10-21
- Volume
- 12
- Issue
- 20
- Pages
- 20728-20742
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC7655176
- OpenAlex
- W3093624462
- Cited by
- 35
- References
- 50
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 6 · 2023: 6 · 2022: 8 · 2021: 8 · 2020: 1
- FWCI
- 3.46
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Aging (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81471352, 81641160)
- Natural Science Foundation of Guangdong Province (No.2018A0303130272, 2018A0303130272, 2016A030313251, No.2016A030313251, 2016A030313827)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- miR-338-5p, BCL2L11, Alzheimer's disease, neuronal apoptosis, amyloid-beta, APP/PS1 mice, amyloid plaques, cognitive impairment, hippocampus
- MeSH terms
- Bcl-2-Like Protein 11, Alzheimer Disease, Animals, Cells, Cultured, Male, Mice, Inbred C57BL, Neurons, Apoptosis, MicroRNAs, Mice, Cognitive Dysfunction
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