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Once any steroid hormone is injected in the body, it binds itself to the specific intracellular receptor of the target cell once it diffuses through the plasma membrane. In the same fashion, androgens combine themselves with a cytosolic (cytosol is the internal fluid of the cell where a greater part of cell metabolism takes place) or nuclear receptor protein once it diffuses across the plasma membrane.

Technically, the androgen receptor is an intracellular steroid receptor whose only function is to bind testosterone and dihydrotestosterone. Androgen receptors have two major forms A and B which only differs in terms of their molecular weight. This androgen-receptor complex goes through a process of conformational changes in the nucleus, which exposes the DNA-binding sites, then binds itself to specific hormone response elements in the DNA. This process results in the dramatic change of the AR-androgen comples (ARAC) which binds into the androgen-responsive elements (ARE). The androgen-responsive elements (ARE) are binding sited in the regions of the DNA where ARAC could attach itself into once it is transported to the nucleus. Many of the bodily proteins contains ARE that are encoded in their DNA which allows androgens easier transcription modulation of the various genes that it can activate or suppress.


The X chromosome has the gene for the androgen receptor located at Xq11-12 and although ongoing researches are suspecting that there are many genes involved in the pattern baldness, there is but one gene that has been properly identified so far with the advances in the research—the AR gene. This AR gene was found out to be the one responsible in enabling the body to make the androgen receptors, which allow the body to respond to dihydrotestosterone and other androgens.

AR Deficiency

The sensitivity of the cells to androgens is attributed to the androgen receptors. There were many genetic mutations that were noted in the gene that encodes the AR in varieties of diseases such as spinal and bulbar muscle atrophy and prostate cancer (besides the androgen insensitivity) – some of which are commonly associated with functional changes in the AR expression. When a particular androgen receptor gene located in the X chromosome mutates due in part by the absence of actively functioning androgen receptors, a medical complication called Androgen resistance syndrome results. When this happens, a genetically male fetus doesn’t undergo normal male development but evolves into a phenotypically female child instead.

It was noted that slight variations in the AR gene causes an increased risk of pattern baldness; and expression of the AR is found in numbers in a balding scalp. However, there is no clear explanation how these genetic changes could increase the risk of patterned hair loss in both men and women. When slight changes occur in the types of DNA building blocks that make up the androgen receptor gene, variations of the AR gene emerges. These changes are frequent in men with premature hair loss. An unknown mechanism triggers the activation of the genes that are responsible for the follicular miniaturization whenever the DHT binds to androgen receptors in susceptible hair follicles – a usual occurrence in the case of bald men. Given this information, it can be hypothesized that the androgen receptor plays a key role in regulating the potency of the available androgen to the hair follicle and thus is an ideal candidate for the involvement in the predisposition to pattern baldness.


The regulation of gene transcription was the first discovered mechanism of action for androgen reactions. Recent studies had shown that androgen-receptors can act independently from their interaction with DNA – since androgen receptors interact only with certain signal transduction protein in the cytoplasm. Signal transduction is the process by which cells convert one kind of signal or stimulus into another.

The direct interaction of androgen receptors with testosterones occurs in some cell types while in others, the testosterone is easily converted by 5-alpha-reductase to dihydrotestosterone, an even more potent agonist in activating androgen receptor. In other words, DHT is produced from testosterone. The order of affinity of the androgen receptor binding in the various steroid hormones is as follows: DHT> testosterone > estrogen > progesterone. The receptor-DHT complex is more stable and can persist longer in cells, making it roughly 3 to 4 times stronger agonist androgen-receptor than testosterone. It has been found out that the DHT is more effective compared to testosterone in the promotion of up-regulation of the androgen receptor. This phenomenon occurs because of the augmentation of the rate of the synthesis of receptors and the inhibition of receptor turn over.

Interaction of DHT with AR and ARE

Evidence points out that DHT triggers the androgen-mediated effects on the hair follicle and the principal signal transduction cascade: DHT-DHT/androgen receptor – ARE is found to be similar in all hair follicles. But study results of pattern baldness have shown that DHT is responsible for the growth of hair follicles, while terminal hairs were found to have been converted into thin vellus hair by miniaturization in other areas. This leaves conclusive proof that there are unknown mechanisms present between hair follicle target-cells in androgen-dependent sites and in androgen-independent growth sites. While no definite explanation exists so far, evidence points to the androgen receptor or distinct ARE involvement in the process.

Distribution of androgen Receptor in hair follicles

Controversy surrounds the documented results on the localization of androgen receptors, and the conflicting results in the quantitative concentrations of androgen receptors in bald versus hairy scalps offer little to assuage the curiosity.

It appears that the androgen receptor is primarily located at the dermal papillae in both anagen and telogen hairs. It is also present in the dermal sheath cells, which supports the concept that the possibility of dermal sheath cells being able to replace dermal papilla cells even in androgen-dependent follicles is considerable. In frontal balding, or Hamilton II to III androgenic alopecia, Saway and Price were able to show a discrepancy of 30% greater in the distribution of androgen receptors in the frontal scalp hair follicles compared to the occipital scalp hair follicles. Randall and colleagues were able to show that there is much higher amount of specific high-affinity, low-capacity androgen receptor in the cultured dermal papillae cells from androgen-dependent sited compared to the non-balding scalp.

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