Progressive Expression Of Ppargc1α Is Associated With Hair Miniaturization In Androgenetic Alopecia | HairLossTalk Forums
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Progressive Expression Of Ppargc1α Is Associated With Hair Miniaturization In Androgenetic Alopecia

Discussion in 'Hair Loss and Alopecia Published Studies' started by whatevr, Jun 25, 2019.

  1. whatevr

    whatevr Senior Member My Regimen

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    https://www.nature.com/articles/s41598-019-43998-7

    Current opinion views androgens as the pathogenic driver in the miniaturization of hair follicles of androgenetic alopecia by interfering with the dermal papilla. This cannot be the sole cause and therefore it is important for therapeutic and diagnostic purposes to identify additional pathways. Comparative full transcriptome profile analysis of the hair bulb region of normal and miniaturized hair follicles from vertex and occipital region in males with and without androgenetic alopecia revealed that next to the androgen receptor as well the retinoid receptor and particularly the PPAR pathway is involved in progressive hair miniaturization. We demonstrate the concurrent up-regulation of PPARGC1a in the epithelial compartment and androgen receptor in the dermal papilla of miniaturized hair. Dynamic Ppargc1a expression in the mouse hair cycle suggests a possible role in regulating hair growth and differentiation. This is supported by reduced proliferation of human dermal papilla and predominantly epithelial keratinocytes after incubation with AICAR, the agonist for AMPK signaling which activates PPARGC1a and serves as co-activator of PPARγ. In addition, miRNA profiling shows enrichment of miRNA-targeted genes in retinoid receptors and PPARGC1α/PPARγ signaling, and antigen presentation pathways.
     
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  2. whatevr

    whatevr Senior Member My Regimen

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    Interestingly enough, in a study posted by another member, AMPK agonist AICAR is claimed to promote hair growth:

    https://www.sciencedirect.com/science/article/pii/S2211124719306990

    However, in this study, AICAR is responsible for the activation of PPARGC1a which the authors claim is associated with miniaturization (in this case, associated merely means they found it upregulated wherever there is miniaturization). Given the above, it is possible that the PPAR upregulation is a protective, rather than causative one. Even the authors of the original study note this:

    "Further work needs to be done to distinguish if PGC1a is involved in Androgenetic Alopecia pathogenesis or plays a protective role against Androgenetic Alopecia."
     
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