MiR34a Regulates Neuronal MHC Class I Molecules and Promotes Primary Hippocampal Neuron Dendritic Growth and Branching
Open accessAbstract
In the immune system, Major Histocompatibility Complex class I (MHC-I) molecules are located on the surface of most nucleated cells in vertebrates where they mediate immune responses. Accumulating evidence indicates that MHC-I molecules are also expressed in the central nervous system (CNS) where they play important roles that are significantly different from their immune functions. Classical MHC-I molecules are temporally and spatially expressed in the developing and adult CNS, where they participate in the synaptic formation, remodeling and plasticity. Therefore, clarifying the regulation of MHC-I expression is necessary to develop an accurate understanding of its function in the CNS. Here, we show that microRNA 34a (miR34a), a brain enriched noncoding RNA, is temporally expressed in developing hippocampal neurons, and its expression is significantly increased after MHC-I protein abundance is decreased in the hippocampus. Computational algorithms identify putative miR34a target sites in the 3'UTR of MHC-I mRNA, and here we demonstrate direct targeting of miR34a to MHC-I mRNA using a dual-luciferase reporter assay system. MiR34a targeting can decrease constitutive MHC-I expression in both Neuro-2a neuroblastoma cells and primary hippocampal neurons. Finally, miR34a mediated reduction of MHC-I results in increased dendritic growth and branching in cultured hippocampal neurons. Taken together, our findings identify miR34a as a novel regulator of MHC-I for shaping neural morphology in developing hippocampal neurons.
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H2-K and H2-D negatively regulate dendritic complexity and the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs) in hippocampal and cortical neurons.
“H2-K and H2-D also negatively regulate dendritic complexity and the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs) in hippocampal and cortical neurons”
From An innate immune response to adeno-associated virus genomes decreases cortical dendritic complexity and disrupts synaptic transmission (2024) · cites this paper as [28]
H2-K and H2-D limit the levels of Ca2+-permeable AMPA receptors in the lateral geniculate nucleus.
“limit the levels of Ca2+-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in the lateral geniculate nucleus.21,22,26,27,28,29”
From An innate immune response to adeno-associated virus genomes decreases cortical dendritic complexity and disrupts synaptic transmission (2024) · cites this paper as [28]
A growing number of immune proteins have been identified that play central roles in neuronal homeostasis, where they negatively regulate neurite length, dendritic complexity, and synaptic transmission, and many are upregulated by TLR9.
“A growing number of immune proteins have been identified that play central roles in neuronal homeostasis, where they negatively regulate neurite length, dendritic complexity, and synaptic transmission,20,21,22,23,24,25,26,27,28,29,45,46,48,72,73,74,75,76,77,78,79 and many are upregulated by TLR9.”
From An innate immune response to adeno-associated virus genomes decreases cortical dendritic complexity and disrupts synaptic transmission (2024) · cites this paper as [28]
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- Authors
- Hu, Y., Pei, W., Hu, Y., Li, P., Sun, C., Du, J., Zhang, Y., Miao, F., Zhang, A., Shen, Y., & Zhang, J.
- Affiliations
- Southeast University (CN)
- Zhongda Hospital Southeast University (CN)
- Corresponding author
- Shen, Yuqing
- Zhang, Jianqiong
- ORCID
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2020-10-28
- Volume
- 14
- Pages
- 573208-573208
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC7655649
- OpenAlex
- W3096772980
- Cited by
- 18
- References
- 41
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 3 · 2022: 2 · 2021: 4
- FWCI
- 0.87
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China
- Graduate Research and Innovation Projects of Jiangsu Province
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- miR-34a, MHC class I, hippocampal neurons, dendritic growth, dendritic branching, microRNA target regulation, 3' untranslated region, neuronal morphology, brain development
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