CoChat
Sign Up
Cited by 32

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Overexpression of miR-132-3p contributes to neuronal protection in in vitro and in vivo models of Alzheimer’s disease

Zeng, Chong, Meng, Xingjun, Mai, Dongmei, Xu, Kai, Qu, Shaogang·2022·Behavioural Brain Research
DOI 10.1016/j.bbr.2021.113584
Open this paper in CoChat — free account

Abstract

One of the neuropathological hallmarks of Alzheimer's disease (AD) is accumulation and deposition of amyloid-beta (Aβ 1-42 ) plaques in the hippocampus. Recently, microRNAs (miRNAs), have been demonstrated to play an essential role in AD. We have previously demonstrated that miR-132-3p exerts neuroprotection via regulating histone deacetylase 3 (HDAC3) in a mouse model of AD. In the present study, we further unveiled neuroprotective roles of miR-132-3p in transgenic amyloid precursor protein/presenilin 1 (APP/PS1) mice compared with those in age-matched wild-type C57BL/6 mice. Lentiviral-mediated inhibition or overexpression of miR-132-3p in the hippocampus of APP/PS1 mice was used to explore the contributions of hippocampal miR-132-3p in spatial memory, amyloid burden, apoptosis, and the number of hippocampal cells in a mouse model of AD. Overexpression of hippocampal miR-132-3p ameliorated spatial memory deficits in the Morris water maze, reduced both Aβ 1-42 accumulation and apoptosis, and promoted the numbers of hippocampal cells in the brains of APP/PS1 mice. Furthermore, trichostatin A (TSA) promoted the expression of miR-132-3p in Aβ 1-42 -burdened neurons while increasing the expression levels of synaptic proteins. Taken together, our results suggest that miR-132-3p may represent a promising therapeutic target for the treatment of AD.

Overview

Integrity signals

Registry

Crossref · 10.1016/j.bbr.2021.113584

Cites

5 of 5 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Show all 5 references

Research works printed but not linked: 46

  1. Hodson, 2018, Alzheimer's disease, Nature, 559, S1, 10.1038/d41586-018-05717-6 · DOI
  2. Janczura, 2018, Inhibition of HDAC3 reverses Alzheimer's disease-related pathologies in vitro and in the 3xTg-AD mouse model, Proc. Natl. Acad. Sci. U. S. A., 115, E11148, 10.1073/pnas.1805436115 · DOI · Paper page
  3. Selkoe, 2016, The amyloid hypothesis of Alzheimer’s disease at 25 years, EMBO Mol. Med., 8, 595, 10.15252/emmm.201606210 · DOI · Paper page
  4. Heneka, 2015, Neuroinflammation in Alzheimer’s disease, Lancet Neurol., 14, 388, 10.1016/S1474-4422(15)70016-5 · DOI · Paper page
  5. Huang, 2018, Magnesium boosts the memory restorative effect of environmental enrichment in Alzheimer’s disease mice, CNS Neurosci. Ther., 24, 70, 10.1111/cns.12775 · DOI
  6. Stoccoro, 2018, Role of epigenetics in Alzheimer’s disease pathogenesis, Neurodegener. Dis. Manag., 8, 181, 10.2217/nmt-2018-0004 · DOI
  7. Peserico, 2011, Physical and functional HAT/HDAC interplay regulates protein acetylation balance, J. Biomed. Biotechnol., 2011
  8. Dagnas, 2013, HDAC inhibition facilitates the switch between memory systems in young but not aged mice, J. Neurosci., 33, 1954, 10.1523/JNEUROSCI.3453-12.2013 · DOI
  9. Zhu, 2017, HDAC3 negatively regulates spatial memory in a mouse model of Alzheimer’s disease, Aging Cell, 16, 1073, 10.1111/acel.12642 · DOI · Paper page
  10. Olde Loohuis, 2012, MicroRNA networks direct neuronal development and plasticity, Cell Mol. Life Sci., 69, 89, 10.1007/s00018-011-0788-1 · DOI
  11. Ai, 2013, MicroRNA-195 protects against dementia induced by chronic brain hypoperfusion via its anti-amyloidogenic effect in rats, J. Neurosci., 33, 3989, 10.1523/JNEUROSCI.1997-12.2013 · DOI
  12. Banzhaf-Strathmann, 2014, MicroRNA-125b induces tau hyperphosphorylation and cognitive deficits in Alzheimer’s disease, EMBO J., 33, 1667, 10.15252/embj.201387576 · DOI · Paper page
  13. Schonrock, 2012, Target gene repression mediated by miRNAs miR-181c and miR-9 both of which are down-regulated by amyloid-beta, J. Mol. Neurosci., 46, 324, 10.1007/s12031-011-9587-2 · DOI
  14. Shaltiel, 2013, Hippocampal microRNA-132 mediates stress-inducible cognitive deficits through its acetylcholinesterase target, Brain Struct. Funct., 218, 59, 10.1007/s00429-011-0376-z · DOI
  15. Salta, 2017, microRNA-132: a key noncoding RNA operating in the cellular phase of Alzheimer’s disease, FASEB J., 31, 424, 10.1096/fj.201601308 · DOI · Paper page
  16. Schröder, 2014, MicroRNA-138 is a potential regulator of memory performance in humans, Front Hum. Neurosci., 8, 501
  17. Hu, 2013, MicroRNA-98 induces an Alzheimer’s disease-like disturbance by targeting insulin-like growth factor 1, Neurosci. Bull., 29, 745, 10.1007/s12264-013-1348-5 · DOI
  18. Geekiyanage, 2011, MicroRNA-137/181c regulates serine palmitoyltransferase and in turn amyloid beta, novel targets in sporadic Alzheimer’s disease, J. Neurosci., 31, 14820, 10.1523/JNEUROSCI.3883-11.2011 · DOI · Paper page
  19. Wei, 2020, Environmental enrichment prevents Aβ oligomer-induced synaptic dysfunction through mirna-132 and hdac3 signaling pathways, Neurobiol. Dis., 134, 10.1016/j.nbd.2019.104617 · DOI
  20. Manterola, 2013, 1-42 β-amyloid peptide requires PDK1/nPKC/Rac 1 pathway to induce neuronal death, Transl. Psychiatry, 3, 219, 10.1038/tp.2012.147 · DOI
  21. Huang, 2018, Increased miR-124-3p in microglial exosomes following traumatic brain injury inhibits neuronal inflammation and contributes to neurite outgrowth via their transfer into neurons, FASEB J., 32, 512, 10.1096/fj.201700673r · DOI · Paper page
  22. Vorhees, 2006, Morris water maze: procedures for assessing spatial and related forms of learning and memory, Nat. Protoc., 1, 848, 10.1038/nprot.2006.116 · DOI · Paper page
  23. Ren, 2016, Therapeutic effects of histone deacetylase inhibitors in a murine asthma model, Inflamm. Res., 65, 995, 10.1007/s00011-016-0984-4 · DOI · Paper page
  24. Manczak, 2011, Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer’s disease: implications for neuronal damage, Hum. Mol. Genet., 20, 2495, 10.1093/hmg/ddr139 · DOI
  25. Benito, 2015, HDAC inhibitor-dependent transcriptome and memory reinstatement in cognitive decline models, J. Clin. Invest., 125, 3572, 10.1172/JCI79942 · DOI
  26. Hansen, 2016, Targeted deletion of miR-132/-212 impairs memory and alters the hippocampal transcriptome, Learn Mem., 23, 61, 10.1101/lm.039578.115 · DOI · Paper page
  27. Wong, 2013, De-repression of FOXO3a death axis by microRNA-132 and -212 causes neuronal apoptosis in Alzheimer’s disease, Hum. Mol. Genet., 22, 3077, 10.1093/hmg/ddt164 · DOI · Paper page
  28. Smith, 2015, miR-132/212 deficiency impairs tau metabolism and promotes pathological aggregation in vivo, Hum. Mol. Genet., 24, 6721, 10.1093/hmg/ddv377 · DOI · Paper page
  29. Xiao, 2019, miR-212-5p attenuates ferroptotic neuronal death after traumatic brain injury by targeting Ptgs2, Mol. Brain, 12, 78, 10.1186/s13041-019-0501-0 · DOI · Paper page
  30. Hadar, 2018, SIRT1, miR-132 and miR-212 link human longevity to Alzheimer's disease, Sci. Rep., 8, 8465, 10.1038/s41598-018-26547-6 · DOI
  31. Cha, 2019, miR-212 and miR-132 are downregulated in neurally derived plasma exosomes of Alzheimer’s patients, Front Neurosci., 13, 1208, 10.3389/fnins.2019.01208 · DOI · Paper page
  32. Aten, 2019, miR-132/212 is induced by stress and its dysregulation triggers anxiety-related behavior, Neuropharmacology, 144, 256, 10.1016/j.neuropharm.2018.10.020 · DOI
  33. Song, 2018, MiR-212 Attenuates MPP?-induced neuronal damage by targeting KLF4 in SH-SY5Y Cells, Yonsei Med J., 59, 416, 10.3349/ymj.2018.59.3.416 · DOI
  34. Hansen, 2016, Targeted deletion of miR-132/-212 impairs memory and alters the hippocampal transcriptome, Learn. Mem., 23, 61, 10.1101/lm.039578.115 · DOI · Paper page
  35. Wang, 2017, Downregulation of miR-132/212 impairs S-nitrosylation balance and induces tau phosphorylation in Alzheimer’s disease, Neurobiol. Aging, 51, 156, 10.1016/j.neurobiolaging.2016.12.015 · DOI · Paper page
  36. Wang, 2020, MicroRNA miR-212 regulates PDCD4 to attenuate Aβ25-35-induced neurotoxicity via PI3K/AKT signaling pathway in Alzheimer’s disease, Biotechnol. Lett., 42, 1789, 10.1007/s10529-020-02915-z · DOI
  37. Wang, 2017, Downregulation of miR-132/212 impairs S-nitrosylation balance and induces tau phosphorylation in Alzheimer’s disease, Neurobiol. Aging, 51, 156, 10.1016/j.neurobiolaging.2016.12.015 · DOI · Paper page
  38. Abel, 2008, Epigenetic targets of HDAC inhibition in neurodegenerative and psychiatric disorders, Curr. Opin. Pharmacol., 8, 57, 10.1016/j.coph.2007.12.002 · DOI
  39. Chuang, 2009, Multiple roles of HDAC inhibition in neurodegenerative conditions, Trends Neurosci., 32, 591, 10.1016/j.tins.2009.06.002 · DOI · Paper page
  40. Zhu, 2014, Histone decacetylase inhibitors prevent mitochondrial fragmentation and elicit early neuroprotection against MPP+, CNS Neurosci. Ther., 20, 308, 10.1111/cns.12217 · DOI
  41. Pichler, 2017, The miRNome of Alzheimer’s disease: consistent downregulation of the miR-132/212 cluster, Neurobiol. Aging, 50, 167
  42. Lau, 2013, Alteration of the microRNA network during the progression of Alzheimer’s disease, EMBO Mol. Med., 5, 1613, 10.1002/emmm.201201974 · DOI · Paper page
  43. Qu, 2019, Ginsenoside Rb1 prevents MPTP-induced changes in hippocampal memory via regulation of the alpha-synuclein/PSD-95 pathway, Aging (Albany N. Y.), 11, 1934
  44. Hansen, 2010, Transgenic miR132 alters neuronal spine density and impairs novel object recognition memory, PLoS One, 5, 15497, 10.1371/journal.pone.0015497 · DOI
  45. El Fatimy, 2018, MicroRNA-132 provides neuroprotection for tauopathies via multiple signaling pathways, Acta Neuropathol., 136, 537, 10.1007/s00401-018-1880-5 · DOI · Paper page
  46. Li, 2019, Developmental neurotoxicity in the context of multiple sevoflurane exposures: Potential role of histone deacetylase 6, Neurotoxicol. Teratol., 74, 10.1016/j.ntt.2019.106813 · DOI

Cited by

Sorted by citations

Metadata

Authors
Zeng, C., Meng, X., Mai, D., Xu, K., & Qu, S.
Venue
Behavioural Brain Research
Publisher
Elsevier BV
Published
2022-01
Volume
417
Pages
113584
ISSN
0166-4328
DOI
10.1016/j.bbr.2021.113584
Cited by
32
References
5
Language
en
Licence
Funders
National Natural Science Foundation of China (81870991, U1603281)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review