75th SID Annual Meeting - May 13, Scottsdale Arizona | HairLossTalk Forums
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75th SID Annual Meeting - May 13, Scottsdale Arizona

Discussion in 'New Research, Studies, and Technologies' started by hellouser, May 1, 2016.

  1. hellouser

    hellouser Senior Member My Regimen

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    InBeforeTheCure likes this.
  2. Noisette

    Noisette Established Member

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    Thanks Hellouser to post it here :) I can't make a thread as I'm a new member.
    But I can post a new thing that i Found and I don't share on BTT, their abstract:

    K. Washenik and Cotsarelis Abstract:
    Prostaglandin D[SUB]2[/SUB] (PGD[SUB]2[/SUB]) and its synthesizing enzyme, PGD[SUB]2[/SUB] synthase, are present at higher levels in balding versus non-balding scalp in men with androgenetic alopecia. Our previous observations (Garza, 2012) in a mouse model that PGD[SUB]2[/SUB] inhibits hair growth via CRTH2/ PTGDR2, one of two PGD[SUB]2[/SUB] receptors, led us to hypothesize that PTGDR2 is the key receptor mediating the hair growth inhibitory activity of PGD[SUB]2[/SUB] in human follicles. In this study we tested several pharmacological PTGDR2 antagonists for their anti-PGD[SUB]2[/SUB] activity on human hair growth in vitro. We found that PTGDR2 antagonists reversed the growth inhibition mediated by PGD[SUB]2[/SUB], in a dose-dependent manner (p<0.01), by reducing PGD[SUB]2[/SUB]-triggered apoptosis and maintaining keratinocyte proliferation. Topical administration of PGD[SUB]2[/SUB] to mice resulted in shortening of the anagen phase and accelerated entry into catagen, while applying a PTGDR2 antagonist to mice extended anagen phase, resulting in longer hair. RNA-Seq analysis on cultured human hair follicles showed decreased expression of hair follicle progenitor cell markers, such as CD34 and K19, in the PGD[SUB]2[/SUB] treated group. FACS analysis of mouse skin cells showed decreased Ki67-positive cells in the secondary hair germ population prior to anagen re-entry in PGD[SUB]2[/SUB] treated mice (p=0.029). These results suggest that PGD[SUB]2[/SUB] suppresses the activation of the secondary germ/ hair progenitor cells. Our findings further underscore the key role of PGD[SUB]2[/SUB] in regulating hair growth and indicate that pharmacological antagonism of PTGDR2 may be an effective approach in preventing and/or treating alopecia in patients sensitive to PGD[SUB]2[/SUB].
     
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  3. InBeforeTheCure

    InBeforeTheCure Established Member My Regimen

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    Interesting. CRTH2, when bound to PGD2, can promote the nuclear translocation of NFATc1.

    [​IMG]

    Fig. 8 – Scheme summarizing the proposed signal
    pathways used by PGD2/CRTH2 to activate human Th2
    cells. Activation of CRTH2 by PGD2 causes separation of
    GTP-bound Gai protein from the receptor and Gbg
    subunits. Consequently Gbg subunits stimulate effector
    molecules, which include PI3Kg and PLCb. Activation of
    PI3Kg leads to phosphorylation of Akt and re-organization
    of cell skeleton including actin polymerization that is
    required by chemotaxis. Inhibition of the PI3K pathway by
    LY294002 attenuates downstream actin polymerization
    and chemotaxis. Gbg-stimulated PLCb generates IP3,
    which elicit Ca2+ influx into the cytosol. Liberated Ca2+
    binds CaM that activates phosphatase calcineurin, which
    in turn dephosphorylates NFAT inducing its activation
    and translocation to the nucleus, and resulting in cytokine
    gene transcription. Inhibition of calcineurin with FK506 or
    CsA blocks NFAT nuclear translocation and cytokine
    production. PI3K signals are also involved in the
    regulation of NFAT via GSK-3b. Activated Akt
    phosphorylates and inactivates GSK-3b. Inhibition of GSK-
    3b phosphorylation promotes NFAT re-phosphorylation
    and nuclear export. Blockade of GSK-3b activity with
    SB216763 prolongs the duration of NFAT nuclear residence
    and enhances gene transcription.

    Source for the above: Inhibition of PI3K and calcineurin suppresses chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2)-dependent responses of Th2 lymphocytes to prostaglandin D(2)

    And...NFATc1 balances quiescence and proliferation of skin stem cells

    Here's another paper showing that nuclear NFAT can bind to Dishevelled (Dvl) and prevent the beta-catenin complex from transcribing its target genes: http://www.jbc.org/content/286/43/37399.full

    So perhaps this is the mechanism by which PGD2 inhibits bulge cell activation. PGD2 binds to CRTH2, which promotes the nuclear translocation of NFAT, preventing bulge cell activation (possibly by binding to Dvl and preventing transcription of Wnt target genes)?

    - - - Updated - - -

    By the way, that second paper shows that NFAT1c can bind to the CDK4 promoter and repress its transcription. This would stop the cell cycle progression from G1 to S independent of any effect on beta-catenin.
     
    I.D WALKER likes this.
  4. HairlossCurse

    HairlossCurse Member

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    Where did you find this abrstract, you sure this isnt from WHC 2015?
     
  5. Noisette

    Noisette Established Member

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  6. Dench57

    Dench57 Senior Member My Regimen

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    Unfortunately it seems 1/3 of people are not sensitive to PGD2.
     
  7. resu

    resu Senior Member

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    I hope those are the ones that don't feel the burning itch.
     
  8. hellouser

    hellouser Senior Member My Regimen

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    Sounds like the Alopecia Areata sufferers where some dont respond to JAK inhibitors. Unless they all do?
     
  9. HairlossCurse

    HairlossCurse Member

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    Yeah its really strange considering the huge direct impact PGD2 has on hair growth
     
  10. Dench57

    Dench57 Senior Member My Regimen

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    You'd have thought so. I have the burning itch but didn't respond to any CRTH2 antagonists. Other inflammatory mediators involved I guess.
     
  11. Tracksterderm

    Tracksterderm Established Member My Regimen

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    There are more interesting things at that event, at page 64 for instance:
    Augmentation of HGF signaling: Potential for enhancing hair follicle neogenesis anddevelopment in bioengineered skin. Rajesh Thangapazham, Ognoon Mungunsukh,Gauthaman Sukumar, Clifton Dalgard, Matthew Wilkerson, Regina Day and Thomas Darling.Bethesda, MD. 3:36 pm, Poster #742
     
  12. Xaser94

    Xaser94 Established Member

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    Rajesh Thangapazham is a very big figure in the hairloss world. I would be very interested in this presentation.

    http://www.hairlosscure2020.com/category/rajesh-thangapazham/
     
  13. Baldybald1

    Baldybald1 Established Member

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    Then we ask again, is follica preparing for a cure ? Maybe yes but they don't want to announce it at this moment !
     
  14. InBeforeTheCure

    InBeforeTheCure Established Member My Regimen

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    Damn, I'd really like to know more about this one:

    - - - Updated - - -

    ^^^ Okay, I've found it! :woot:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826467/
     
  15. HairlossCurse

    HairlossCurse Member

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    Now that the meeting is done, does anyone know if any information will be released?
     

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