Article Synopsis
- Androgenetic alopecia (AGA) is a hereditary hair loss condition in men linked to certain genetic risk factors, with 12 known loci but unclear specific genes involved.
- Immortalized dermal papilla cells (DPCs), derived from balding and non-balding scalps, were found to preserve key signature characteristics and were used to analyze gene expression.
- The study identified AR as a potential candidate gene at one AGA risk locus and highlighted TWIST1 and SSPN as functionally relevant genes at two others, indicating that reduced vascular-related gene activity in balding scalps could contribute to AGA development.
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Article Abstract
Androgenetic alopecia (AGA) is a common heritable and androgen-dependent hair loss condition in men. Twelve genetic risk loci are known to date, but it is unclear which genes at these loci are relevant for AGA. Dermal papilla cells (DPCs) located in the hair bulb are the main site of androgen activity in the hair follicle. Widely used monolayer-cultured primary DPCs in hair-related studies often lack dermal papilla characteristics. In contrast, immortalized DPCs have high resemblance to intact dermal papilla. We derived immortalized human DPC lines from balding (BAB) and non-balding (BAN) scalp. Both BAB and BAN retained high proportions of dermal papilla signature gene and versican protein expression. We performed expression analysis of BAB and BAN and annotated AGA risk loci with differentially expressed genes. We found evidence for AR but not EDA2R as the candidate gene at the AGA risk locus on chromosome X. Further, our data suggest TWIST1 (twist family basic helix-loop-helix transcription factor 1) and SSPN (sarcospan) to be the functionally relevant AGA genes at the 7p21.1 and 12p12.1 risk loci, respectively. Down-regulated genes in BAB compared to BAN were highly enriched for vasculature-related genes, suggesting that deficiency of DPC from balding scalps in fostering vascularization around the hair follicle may contribute to the development of AGA.
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| http://dx.doi.org/10.1016/j.jid.2016.03.032 | DOI Listing |
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