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miR-211-5p targeting MMP9 regulates the expressions of AQP4 in traumatic brain injury

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Abstract

Objective

The abnormal expression of matrix metalloproteinase 9 (MMP9) and Aquaporin 4 (AQP4) closely associates with the traumatic brain injury (TBI) development.

Methods

Here, we investigated the relationship between miR-211-5p and MMP9/AQP4 axis in TBI patients and astrocyte cells. Demographics, clinical features, and cerebrospinal fluid (CSF) samples were collected from traumatic brain injury (TBI) patients (n = 96) and controls (n = 30) for pathological and gene expression analyses. Luciferase activity assay and gene expression analyses were performed to dissect the regulatory mechanism of miR-211-5p on MMP9/AQP4 in human astrocyte cells.

Results

miR-211-5p mRNA was significantly decreased in the CSF of TBI patients, which positively correlated with the expression of both MMP9 and AQP4. miR-211-5p could target MMP9 directly in SVG P12 cells. Overexpression of miR-211-5p decreased the expression of MMP9, on the contrary, knockdown miR-211-5p through inhibitors increased the expression of both MMP9 and AQP4.

Conclusion

miR-211-5p inhibits the MMP9/AQP4 axis in human astrocyte cells, which represents a promising approach for the TBI treatment.

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Funding

The study was supported by Natural Science Foundation of Hebei Province (HH2020206543).

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Correspondence to Lijun Yang or Zhenzeng Fan.

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The authors have no conflicts of interest to declare.

Ethical approval

All procedures perfomed in this study involving human participants were in accordance with the Declaration of Helsinki, Ethical Principles for Medical Research Involving Human Subjects, and approved by the Second Hospital of Hebei Medical University’s Medical Ethics Board (#2022-R258).

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The written informed consent was obtained from all the participants of this study.

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Wang, M., Yu, X., Li, B. et al. miR-211-5p targeting MMP9 regulates the expressions of AQP4 in traumatic brain injury. Acta Neurol Belg 123, 1321–1329 (2023). https://doi.org/10.1007/s13760-023-02205-1

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  • DOI: https://doi.org/10.1007/s13760-023-02205-1

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