New Paper From Tokyo University About Dpcs And Dscs Hair-inductive Capacity

Joxy

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Hair regeneration potential of human dermal sheath cells cultured under physiological oxygen

We investigated the effect of oxygen tension on the proliferation and hair-inductive capacity of human dermal papilla cells (DPCs) and dermal sheath cells (DSCs). DPCs and DSCs were separately obtained from human hair follicles and each cultured under atmospheric/hyperoxic (20% O2), physiological/normoxic (6% O2), or hypoxic (1% O2) conditions. Proliferation of DPCs and DSCs was highest under normoxia. Compared to hyperoxia, hypoxia inhibited the proliferation of DPCs but enhanced that of DSCs. In DPCs, hypoxia down-regulated the expression of hair-inductive capacity-related genes, including BMP4, LEF1, SOX2, and VCAN. In DSCs, both normoxia and hypoxia up-regulated SOX2 expression, whereas hypoxia down-regulated BMP4 expression. Microarray analysis revealed that normoxia increased the expression of pluripotency-related genes, including SPRY, NR0B1, MSX2, IFITM1, and DAZL compared to hyperoxia. In an in vivo hair follicle reconstitution assay, cultured DPCs and DSCs were transplanted with newborn mouse epidermal keratinocytes into nude mice using a chamber method. In this experiment, normoxia resulted in the most efficient induction of DPC hair follicles, whereas hypoxia caused the most efficient induction and maturation of DSC hair follicles. These results suggest that application of physiological/hypoxic oxygen tension to cultured human DSCs enhances the proliferation and maintenance of hair inductivity for skin engineering and clinical applications.

https://www.liebertpub.com/doi/10.1089/ten.TEA.2019.0329

The most interesting part:

„These results suggest that application of physiological/hypoxic oxygen tension to cultured human DSCs enhances the proliferation and maintenance of hair inductivity for skin engineering and clinical applications.“

But in the end it is still mouse...We don’t know if this will work on humans.
 

pegasus2

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Never was

I wouldn't say that. I'm going to stick with stemoxydine in my regimen, but I'd like to see the mechanisms here elucidated.

Stemoxydine doesn't actually induce hypoxia, it just upregulates HIF-1a which mediates the proliferative effects of hypoxia. Whatever is going on in DPCs here is probably mediated by hypoxia itself not the protective response to it.

Hypoxia-enhanced proliferation and migration of ORS cells were suppressed either by HIF-1α siRNA or by pharmacological inhibitors of Shh pathway, cyclopamine and GANT61. The activation of Shh pathway was attenuated in HIF-1α-silenced ORS cells under hypoxic condition.
https://www.ncbi.nlm.nih.gov/pubmed/29030089
 
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badhabiz

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I wouldn't say that. I'm going to stick with stemoxydine in my regimen, but I'd like to see the mechanisms here elucidated.

Stemoxydine doesn't actually induce hypoxia, it just upregulates HIF-1a which mediates the proliferative effects of hypoxia. Whatever is going on in DPCs here is probably mediated by hypoxia itself not the protective response to it.


https://www.ncbi.nlm.nih.gov/pubmed/29030089
yes, could be, but is has been around for a decade (at least here in europe) never heard a good report tho
 
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