Inhibition Of Trpv3 As A New Therapy For Hair Loss?

[Koga]

https://www.ncbi.nlm.nih.gov/pubmed/31152005

Abstract:

"Hair growth starts from hair follicles that reside in dermis, and abnormal hair growth is an early sign of hair follicle disease or systemic illness such as alopecia or hair loss. Therefore, identifying a target critical for dysfunctional hair follicles is fundamental to alleviating dermatologic or systemic diseases with hair abnormalities. The warm temperature-activated Ca2+-permeable TRPV3 channel protein is abundantly expressed in the skin keratinocytes, and dysfunctional TRPV3 causes human congenital Olmsted syndrome characterized by skin diseases and alopecia, indicating an important role of TRPV3 in hair follicle development and hair growth. To validate TRPV3 as a therapeutic target, we investigated the impact of pharmacological modulation of TRPV3 on hair growth using a combination of biochemical and cell biology, immunohistochemical, whole-cell patch clamp, RNA interference and pharmacological approaches. We find that functional TRPV3 channel proteins are highly expressed in hair follicle outer root sheath (ORS) cells as detected by Western blot analysis, immunohistochemical staining and electrophysiological techniques. Pharmacological activation of TRPV3 by agonist natural carvacrol induces cell death of ORS cells and topical application of carvacrol to mouse dorsal skin also inhibits hair growth. Conversely, specific inhibition of TRPV3 by inhibitor natural forsythoside B (FB) and shRNA reverses the cell death induced by carvacrol-mediated TRPV3 activation in human ORS cells. Furthermore, forsythoside B results in a significant reversal of hair growth inhibition induced by agonist carvacrol. Altogether, our findings demonstrate that TRPV3 channel is critical for regulation of hair growth, and inhibition of TRPV3 may represent a promising therapy for hair loss or hair follicle-related skin diseases."

Anyone seen this? A study from 31th of may 2019.

 

[kiwipilu]

new finding is better than finding nothing as It looks like a step in the right direction but…
It’s « funny » how many pathways regulation could give regrowth and are said to be critical for hair cycle. Actually we can’t even count the studies because there are so many of them. XXX channel, XXX gene, XXX pathway, XXX protein etc. are “critical/key for hair growth” … So which one of them is really that critical?
that said it looks like most don’t work on human with androgenetic alopecia. Or the findings get lost in a galaxy far, far away.

 

[Left4bald]

Here is the full pdf for this new findings : http://jpet.aspetjournals.org/content/jpet/early/2019/05/31/jpet.119.258087.full.pdf

They talked about a Topical carvacrol

" To examine the impact of TRPV3 modulation on hair growth, we carried out topical applications of different concentrations of carvacrol (19.1, 63.7 and 191.1 mM in 150 μl) to the shaved dorsal area (2.5 cm × 3.5 cm) of the skin once a day (Fig. 3A top panel, n=8), and evaluated the time-dependent hair growth by observing the skin black pigmentation and hair growth (Fig. 3A). Black pigmentation in the skin is considered as a transition from telogen to anagen phase (Paus and Cotsarelis, 1999; Paus and Foitzik, 2010).

We observed the three sequential stages of hair growth: pink skin turning black, black skin growing hair and full hair (Fig. 3A and Table 1). Topical applications of TRPV3 agonist carvacrol (19.1, 63.7 and 191.1 mM) caused a concentration-dependent delay of pink skin turning black from day 9 to day 12 (Fig. 3A and Table 1), as compared with the blank control (50% ethanol) or 0.3 mM forsythoside B group that exhibited a visible black coloration on day 9 (Fig. 3A). Similarly, topical applications of carvacrol (19.1, 63.7 and 191.1 mM) also caused a concentration-dependent delay of black skin starting to grow hairs from day 12 to day 15 (Fig. 3A), as compared with blank control or forsythoside B group that started to grow hairs on day 12 (Fig. 3A and Table 1). For measurement of hair length, applications of carvacrol (19.1, 63.7 and 191.1 mM) resulted in concentration-dependent reduction of hair length, as compared with blank control or 0.3 mM forsythiaside B (FB) group (Fig. 3A and 3B).
These results indicate that activation of TRPV3 by carvacrol inhibits hair growth in both time- and concentration-dependent manner ".

 

[Jakejr]

So Carvacrol inhibits hair growth.
Where is anti-Carvacrol...?

 

[Mandar kumthekar]

I think some mysterious thing is behind the baldness that could not be detectable to us.

 

[Jakejr]

Perhaps, but it involves manipulation of hormones & Administration of drugs.
Because of side effects major pharmaceuticals are reticent.
We find hair color, growth, thickness is a very sensitive thing. It’s a marker of health probably genetically to opposite sex.

 

[Left4bald]

So Carvacrol inhibits hair growth.
Where is anti-Carvacrol...?

Your answer is in the study please read it : it's Forsythoside B

" Pharmacological inhibition of overactive TRPV3 by forsythoside B can reverse hair loss. "

Full Study : http://jpet.aspetjournals.org/content/jpet/early/2019/05/31/jpet.119.258087.full.pdf

 

[Koga]

Thank you, Left4bald!

So apparently the source for forsythoside B is (the fruits of) the forsythia suspensa plant. So we might give that, topically, a shot?

https://www.amazon.com/Forsythia-Extract-Suspensa-Tincture-Supplement/dp/B00LC62J7S?th=1

 

[EndlessPossibilities]

Thank you, Left4bald!

So apparently the source for forsythoside B is (the fruits of) the forsythia suspensa plant. So we might give that, topically, a shot?

https://www.amazon.com/Forsythia-Extract-Suspensa-Tincture-Supplement/dp/B00LC62J7S?th=1

Pointless. carvacrol isn’t even made in the body. So why do u even want to inhibit it with a chemical that can’t even penetrate the skin lol.

Find one source that says carvacrol is made in the body and I’ll consider ur thoughts.

 

[zaman]

Does this have something to do with quercetin again?