Retinoic Acid-Related Orphan Receptor Alpha May Regulate the State of Hair Follicle Stem Cells by Upregulating the Expression of BNIP3
The hair, an exclusive keratinized dermal appendage in mammals, stands as a quintessential outcome of adaptive evolution, conferring resilience against adverse environmental conditions. The ontogenesis of the coat displays a pronounced rhythmic pattern, with hair follicle stem cells (HFSCs) emerging...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2024-12-01
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| Series: | Animals |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2076-2615/14/23/3477 |
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| Summary: | The hair, an exclusive keratinized dermal appendage in mammals, stands as a quintessential outcome of adaptive evolution, conferring resilience against adverse environmental conditions. The ontogenesis of the coat displays a pronounced rhythmic pattern, with hair follicle stem cells (HFSCs) emerging as pivotal facilitators of hair follicle reconstitution. The retinoic acid-related orphan receptor alpha, a nuclear receptor with extensive involvement in the regulation of cellular physiological states, exerts its functions predominantly through the modulation of downstream target gene transcription. The <i>Bnip3</i> gene exhibits a robust correlation with cellular apoptosis and autophagy, which are indispensable physiological mechanisms underlying the maintenance of HFSC homeostasis. Consequently, the expression level of <i>Bnip3</i> may be intimately linked to the status of HFSCs. In this investigative endeavor, we employed rat HFSCs as a model system to validate the regulatory impact of RORA on <i>Bnip3</i> gene expression. Our findings unequivocally demonstrate that <i>Bnip3</i> serves as a direct downstream target of RORA. Specifically, RORA binds to the motif within the <i>Bnip3</i> promoter region, thereby upregulating <i>Bnip3</i> expression levels. In light of our research findings, we propose that RORA holds potential as a target for modulating the status of HFSCs. |
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| ISSN: | 2076-2615 |