Midnolin gene expression is enhanced by Gq-coupled muscarinic acetylcholine receptor stimulation in SH-SY5Y human neuroblastoma cells

We previously demonstrated that the midnolin gene (MIDN) is a risk factor for Parkinson's disease (PD) in Yamagata and British cohorts, and that neurite outgrowth is abolished by MIDN knockout in PC12 cells. Therefore, drugs that upregulate MIDN may have neurotrophic effects. In this study, acetylcholine increased MIDN promoter activity and gene expression in a concentration-dependent manner in SH-SY5Y cells. These effects were suppressed by atropine and a G<sub>q</sub> inhibitor, YM254890, indicating that muscarinic receptor/G<sub>q</sub> signaling is required for the induction of MIDN by acetylcholine. Our findings suggest that drugs that upregulate MIDN may have therapeutic potential for PD.

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Publication Details

Journal
Journal of Pharmacological Sciences
Published
2025-02-23
DOI
https://doi.org/10.1016/j.jphs.2025.02.006
Citations
1
Primary Topic
Receptor Mechanisms and Signaling
Type
article
Field-Weighted Citation Impact
0.81

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article

Midnolin gene expression is enhanced by Gq-coupled muscarinic acetylcholine receptor stimulation in SH-SY5Y human neuroblastoma cells

Ikuo Norota, Hiroaki Yamaguchi, Ayano Chiba, Yutaro Obara et al.
1 citations
Journal of Pharmacological Sciences
Receptor Mechanisms and Signaling
0.81
article

Midnolin gene expression is enhanced by Gq-coupled muscarinic acetylcholine receptor stimulation in SH-SY5Y human neuroblastoma cells

Ikuo Norota, Hiroaki Yamaguchi, Ayano Chiba, Yutaro Obara, Jiro Ogura, Mikako Nagashima, Kuniaki Ishii, Yusuke Zuiki
article en
1 citations

Abstract

We previously demonstrated that the midnolin gene (MIDN) is a risk factor for Parkinson's disease (PD) in Yamagata and British cohorts, and that neurite outgrowth is abolished by MIDN knockout in PC12 cells. Therefore, drugs that upregulate MIDN may have neurotrophic effects. In this study, acetylcholine increased MIDN promoter activity and gene expression in a concentration-dependent manner in SH-SY5Y cells. These effects were suppressed by atropine and a G<sub>q</sub> inhibitor, YM254890, indicating that muscarinic receptor/G<sub>q</sub> signaling is required for the induction of MIDN by acetylcholine. Our findings suggest that drugs that upregulate MIDN may have therapeutic potential for PD.

Journal of Pharmacological SciencesVol. 157(4)
Yamagata University (JP)
Takeda Science Foundation, Japan Society for the Promotion of Science
Zero hunger
Openalex Percentile: Top 31%
Receptor Mechanisms and Signaling
0.81
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