Progenitor Cell Dynamics in Androgenetic Alopecia: Insights from Spatially Resolved Transcriptomics
Issued Date
2025-06-01
Resource Type
ISSN
16616596
eISSN
14220067
Scopus ID
2-s2.0-105008955891
Journal Title
International Journal of Molecular Sciences
Volume
26
Issue
12
Rights Holder(s)
SCOPUS
Bibliographic Citation
International Journal of Molecular Sciences Vol.26 No.12 (2025)
Suggested Citation
Charoensuksira S., Surinlert P., Krajarng A., Nualsanit T., Payuhakrit W., Panpinyaporn P., Khumsri W., Thanasarnaksorn W., Suwanchinda A., Hongeng S., Ponnikorn S. Progenitor Cell Dynamics in Androgenetic Alopecia: Insights from Spatially Resolved Transcriptomics. International Journal of Molecular Sciences Vol.26 No.12 (2025). doi:10.3390/ijms26125792 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/111011
Title
Progenitor Cell Dynamics in Androgenetic Alopecia: Insights from Spatially Resolved Transcriptomics
Corresponding Author(s)
Other Contributor(s)
Abstract
Androgenetic alopecia (AGA) is marked by the progressive miniaturization of hair follicles (HFs) and hair thinning, driven by a decline in the progenitor cells critical for hair regeneration. Despite this, the mechanisms responsible for progenitor cell depletion remain largely unclear. To investigate transcriptional alterations in the progenitor cell regions of AGA patients while maintaining the spatial tissue context, we employed the GeoMX Digital Spatial Profiling (DSP) platform, which enables a precise comparison with healthy controls. Our analysis revealed the significant upregulation of genes associated with extracellular matrix (ECM) organization and the epithelial–mesenchymal transition (EMT), including FN1, TWIST1, and TGFB2 in the progenitor cell region of the HFs. Correspondingly, protein expression data confirmed increased levels of the protein products of these genes in the affected areas, underscoring their roles in the disease’s progression. These molecular changes suggest an environment conducive to the EMT, potentially contributing to the loss of progenitor cells and indicating a fibrogenic shift within the HF microenvironment. Additionally, our study highlights the influence of peri-infundibular immune cell infiltration on these molecular changes, suggesting that immune-mediated microinflammation may contribute to the fibrogenic environment and progenitor cell loss in the AGA. These findings demonstrate the utility of spatial transcriptomics in identifying potential therapeutic targets and advancing our understanding of AGA’s molecular mechanisms, offering avenues for developing targeted treatment strategies.