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Regulation of Zbp1 by miR-99b-5p in microglia controls the development of schizophrenia-like symptoms in mice

Kaurani, Lalit, Islam, Md Rezaul, Heilbronner, Urs, Krüger, Dennis M, Zhou, Jiayin, Methi, Aditi, Strauss, Judith, Pradhan, Ranjit, Schröder, Sophie, Burkhardt, Susanne, Schuetz, Anna-Lena, Pena, Tonatiuh, Erlebach, Lena, Bühler, Anika, Budde, Monika, Senner, Fanny, Kohshour, Mojtaba Oraki, Schulte, Eva C, Schmauß, Max, Reininghaus, Eva Z, Juckel, Georg, Kronenberg-Versteeg, Deborah, Delalle, Ivana, Odoardi, Francesca, Flügel, Alexander, Schulze, Thomas G, Falkai, Peter, Sananbenesi, Farahnaz, Fischer, Andre·2024·The EMBO Journal
DOI 10.1038/s44318-024-00067-8PMC PMC11021462
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Abstract

Current approaches to the treatment of schizophrenia have mainly focused on the protein-coding part of the genome; in this context, the roles of microRNAs have received less attention. In the present study, we analyze the microRNAome in the blood and postmortem brains of schizophrenia patients, showing that the expression of miR-99b-5p is downregulated in both the prefrontal cortex and blood of patients. Lowering the amount of miR-99b-5p in mice leads to both schizophrenia-like phenotypes and inflammatory processes that are linked to synaptic pruning in microglia. The microglial miR-99b-5p-supressed inflammatory response requires Z-DNA binding protein 1 (Zbp1), which we identify as a novel miR-99b-5p target. Antisense oligonucleotides against Zbp1 ameliorate the pathological effects of miR-99b-5p inhibition. Our findings indicate that a novel miR-99b-5p-Zbp1 pathway in microglia might contribute to the pathogenesis of schizophrenia.

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  • Even in a large recent study in which 573 blood samples and 30 postmortem brains of schizophrenia patients and controls were analyzed by smallRNAseq, no de-regulation of miR-129 was observed.

    “Even in a large recent study in which 573 blood samples and 30 postmortem brains of schizophrenia patients and controls were analyzed by smallRNAseq, no de-regulation of miR-129 was observed [29].”

    From A role for astrocytic miR-129-5p in frontotemporal dementia (2025) · cites this paper as [29]

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Authors
Kaurani, L., Islam, M. R., Heilbronner, U., Krüger, D. M., Zhou, J., Methi, A., Strauss, J., Pradhan, R., Schröder, S., Burkhardt, S., Schuetz, A.-L., Pena, T., Erlebach, L., Bühler, A., Budde, M., Senner, F., Kohshour, M. O., Schulte, E. C., Schmauß, M., Reininghaus, E. Z., Juckel, G., Kronenberg-Versteeg, D., Delalle, I., Odoardi, F., Flügel, A., Schulze, T. G., Falkai, P., Sananbenesi, F., & Fischer, A.
ORCID
Venue
The EMBO Journal
Publisher
Springer Science and Business Media LLC
Published
2024-03-25
Volume
43
Issue
8
ISSN
1460-2075
DOI
10.1038/s44318-024-00067-8
PMC
PMC11021462
Cited by
17
References
8
Language
en
Licence
Funders
  • Deutsche Forschungsgemeinschaft (SPP1738,SFB1286,EXC 2067/1,EPIFUS, SCHU 1603/4-1,5-1,7-1, GRK2824, 514201724, FA 241/16-1)
  • EC | Horizon 2020 Framework Programme (PSY-PGx,grant agreement No 945151)
  • Bundesministerium für Bildung und Forschung (ERA-NET Neuron EPINEURODEVO, GoBIO, 01EE1404H)
  • EU Joint Programme - Neurodegenerative Disease Research (EPI-3E)
  • Studienstiftung des Deutschen Volkes (Fellowship)
  • IMPRS-MMFD (Fellowship)
  • Chan Zuckerberg Initiative ((2020-221779(5022) & 2021-235147))
  • IMPRS-GS (Fellowship)
  • IMPRS-Neuroscience (Fellowship)
  • Dr. Lisa Oehler Foundation (Fellowship)

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