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Corrigendum Open Access | 10.1172/JCI168441

Aberrant miR-339-5p/neuronatin signaling causes prodromal neuronal calcium dyshomeostasis in mutant presenilin mice

Hao-Yu Zou, Lin Guo, Bei Zhang, Si Chen, Xin-Rong Wu, Xian-Dong Liu, Xin-Yu Xu, Bin-Yin Li, Shengdi Chen, Nan-Jie Xu, and Suya Sun

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Published February 1, 2023 - More info

Published in Volume 133, Issue 3 on February 1, 2023
J Clin Invest. 2023;133(3):e168441. https://doi.org/10.1172/JCI168441.
© 2023 Zou et al. This work is licensed under the Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
Published February 1, 2023 - Version history
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Aberrant miR-339-5p/neuronatin signaling causes prodromal neuronal calcium dyshomeostasis in mutant presenilin mice
Hao-Yu Zou, … , Nan-Jie Xu, Suya Sun
Hao-Yu Zou, … , Nan-Jie Xu, Suya Sun
Research Article Cell biology Neuroscience

Aberrant miR-339-5p/neuronatin signaling causes prodromal neuronal calcium dyshomeostasis in mutant presenilin mice

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Abstract

Mushroom spine loss and calcium dyshomeostasis are early hallmark events of age-related neurodegeneration, such as Alzheimer’s disease (AD), that are connected with neuronal hyperactivity in early pathology of cognitive brain areas. However, it remains elusive how these key events are triggered at the molecular level for the neuronal abnormality that occurs at the initial stage of disease. Here, we identify downregulated miR-339-5p and its upregulated target protein, neuronatin (Nnat), in cortex neurons from the presenilin-1 M146V knockin (PSEN1-M146V KI) mouse model of familial AD (FAD). Inhibition of miR-339-5p or overexpression of Nnat recapitulates spine loss and endoplasmic reticulum calcium overload in cortical neurons with the PSEN1 mutation. Conversely, either overexpression of miR-339-5p or knockdown of Nnat restores spine morphogenesis and calcium homeostasis. We used fiber photometry recording during the object-cognitive process to further demonstrate that the PSEN1 mutant causes defective habituation in neuronal reaction in the retrosplenial cortex and that this can be rescued by restoring the miR-339-5p/Nnat pathway. Our findings thus reveal crucial roles of the miR-339-5p/Nnat pathway in FAD that may serve as potential diagnostic and therapeutic targets for early pathogenesis.

Authors

Hao-Yu Zou, Lin Guo, Bei Zhang, Si Chen, Xin-Rong Wu, Xian-Dong Liu, Xin-Yu Xu, Bin-Yin Li, Shengdi Chen, Nan-Jie Xu, Suya Sun

×

Original citation: J Clin Invest. 2022;132(8):e149160. https://doi.org/10.1172/JCI149160

Citation for this corrigendum: J Clin Invest. 2023;133(3):e168441. https://doi.org/10.1172/JCI168441

The left panel of Figure 5G originally showed a histogram that was inadvertently duplicated from Figure 5E. The correct figure panel is shown below, and the HTML and PDF versions have been updated online. The correction does not affect the results or conclusions of the article.

The authors regret the error.

Footnotes

See the related article at Aberrant miR-339-5p/neuronatin signaling caused prodromal neuronal calcium dyshomeostasis in mutant presenilin mice.

Version history
  • Version 1 (February 1, 2023): Electronic publication

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