Dermal Papilla Androgen Sensitivity, Androgen Receptors & Methylation

Due to the understanding of male pattern baldness as Androgenic Alopecia (i.e. as an androgen-dependent process), many studies have focused on androgen metabolism (AM) in the body and how androgens effect hair.  Studies have shown that “all dermal papilla cells from androgen-sensitive sites contain low capacity, high affinity androgen receptors.” [18]

The dermal papilla (DP), at the base of the hair follicle, has androgen receptors (AR’s) that androgens from the blood bind to. In androgen-sensitive follicles, the androgens are synthesized and diffused over small distances; this induces changes in neighboring cells (like keratinocytes cells) in what is known as “paracrine interactions”. The diffusible proteins are called paracrine factors. [18]

When beard and scalp cells were incubated in androgens, androgens stimulated the cells’ ability to triggered mitosis (cell division) in beard cells but not in scalp cells. The interesting outcome here was that incubation with androgens had the exact opposite effect on scalp cells; these (scalp) cells’ mitogenic capacity was inhibited. [18]

Androgen-sensitive follicles are not simply targeted and affected by androgens; they are actually involved in androgen metabolism (AM) and can convert androgens using steroid-producing (steroidogenic) enzymes, also known as intrafollicular steroidogenic enzymes. [25]

A 2004 study shed more light on specific processes that shorten the hair cycle (that occur within the DP). According to the study, the three processes are as follows: “(1) the conversion of testosterone to DHT by type II 5-alpha-reductase; (2) the synthesis of TGF-beta2 in dermal papilla cells; and (3) the activation of the intrinsic caspase network.” [6]

The research seems to indicate AM activity at the DP of the hair follicle, amongst other interactions is not fully understood yet. Some of the known intrafollicular steroidogenic enzymes found in the DP are: Steroid Sulfatase (STS), 17beta-hydroxysteroid dehydrogenases (17b-HSD), 3beta-hydroxysteroid dehydrogenases (3b-HSD)  and type 1 and 2 5alpha-reductase (type 1 and type 2 5alpha-R). Type 2 5-alpha-reductase has been the target of a number of studies that showed it to accelerate the conversion of free testosterone into DHT. [10] [11] [12] [24] [25] [28] [31]

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Androgen metabolism (AM) within the hair follicle is pivotal in the conversion of weak androgens to potent androgens such dihydrotestosterone (DHT) which is an “active metabolite of testosterone”. This is how testosterone (T) is converted to DHT in the hair follicle itself; thus, intrafollicular steroidogenic enzymes are considered targets for medication or pharmaceutical research in the field of AGA.  [10] [11] [12] [24] [25] [28]

This study Evidence of increased DNA methylation of the androgen receptor gene in occipital hair follicles from men with androgenetic alopecia shows the AR gene activity in men with AGA. Occipital hair follicles in AGA are properly methylated, however the vulnerable MPB hair follicles are not. This sensitivity to steroid hormones results from reduced AR “gene methylation pattern”.

One of the things that epigenetically silence the DKK-1 gene is methylation.

This study discusses hypermethylation Impact of inflammation on epigenetic DNA methylation – a novel risk factor for cardiovascular disease?. It is possible that those who are hypermethylators will have the opposite problem to the majority, and that’s when MSM, and SAM-e might help. Most people would benefit from extra methylation.

Read more on Methylation an hypomethylation here: Methylation and Hair Loss






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