Interesting study on inflammation genes causing hairloss in Androgenetic Alopecia
http://www.bbmt.org/article/S0022-202X(17)33139-1/pdf
http://www.bbmt.org/article/S0022-202X(17)33139-1/pdf
Genes Regulating Inflammation, Stress, And Fibrosis Were Massively Overexpressed In All Androgenetic Alopecia Groups
- Thread starter Warmer82
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Abstract
In most stem cell systems, the organization of the stem cell niche and the anchoring matrix required for stem cell maintenance are largely unknown. We report here that collagen XVII (COL17A1/BP180/BPAG2), a hemidesmosomal transmembrane collagen, is highly expressed in hair follicle stem cells (HFSCs) and is required for the maintenance not only of HFSCs but also of melanocyte stem cells (MSCs), which do not express Col17a1 but directly adhere to HFSCs. Mice lacking Col17a1 show premature hair graying and hair loss. Analysis of Col17a1-null mice revealed that COL17A1 is critical for the self-renewal of HFSCs through maintaining their quiescence and immaturity, potentially explaining the mechanism underlying hair loss in human COL17A1 deficiency. Moreover, forced expression of COL17A1 in basal keratinocytes, including HFSCs, in Col17a1-null mice rescues MSCs from premature differentiation and restores TGF-β signaling, demonstrating that HFSCs function as a critical regulatory component of the MSC niche.
In most stem cell systems, the organization of the stem cell niche and the anchoring matrix required for stem cell maintenance are largely unknown. We report here that collagen XVII (COL17A1/BP180/BPAG2), a hemidesmosomal transmembrane collagen, is highly expressed in hair follicle stem cells (HFSCs) and is required for the maintenance not only of HFSCs but also of melanocyte stem cells (MSCs), which do not express Col17a1 but directly adhere to HFSCs. Mice lacking Col17a1 show premature hair graying and hair loss. Analysis of Col17a1-null mice revealed that COL17A1 is critical for the self-renewal of HFSCs through maintaining their quiescence and immaturity, potentially explaining the mechanism underlying hair loss in human COL17A1 deficiency. Moreover, forced expression of COL17A1 in basal keratinocytes, including HFSCs, in Col17a1-null mice rescues MSCs from premature differentiation and restores TGF-β signaling, demonstrating that HFSCs function as a critical regulatory component of the MSC niche.
Could be possible that because only those cells are prone to the inflammation, dht is used as the body's way to regulate them?
infinitepain
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At the same time, it is known that collagen buildup, turning into so called hard collagen, promotes fibrosis, so minoxidil works in part because it breaks this hard collagen. Balding is nature's troll job.
infinitepain
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What about high DHT men with NW0's.
I don't think DHT is the underlying cause of hair loss. I always think its inflammation either thats down to a mutated faulty hair follicle gene or multiple, or a lack of a protein that protects the the HFSC.
In Androgenetic Alopecia ,Why does COL17A1 breakdown and lead to HFSC aging and epidermal differentiation, thereby causing hair follicle miniaturization
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Put those on the 300 Androgenetic Alopecia potential identified genes
Pump up those numbers
Pump up those numbers
inmyhead
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These are interesting observations. At present, it's much too simple to say that adding back collagen 17 A1 to the scalp will promote hair growth. The Collagen 17 A 1 protein is a complex protein that integrates in the cell membrane of cells and so simply injecting it is unlikely to do much. However, this study reminds us that understanding stem cell aging is likely to yield some of the most important findings to better understand hair loss. -
https://donovanmedical.com/hair-blog/col17a1#sthash.EfuR2A0N.dpuf
First one . DHT is used as an anti inflammatory by the body.
FCKW36
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Than why should blovking DHT help.
Guess we will never know unless we try it.
Finisteride and minoxidil were accidental hair loss drugs. still we dont know exactly how they work. Know one has developed a cure yet, it still may be found by trialling new things
Because its the DHT that does the damage. Inflammation comes > body then uses DHT locally as anti inflammatory and damages follicles. If you have no inflammation you're likely not losing hair the same rate, or if you have no DHT you wont lose hair either.