End of baldness? Scientists spot key chemical that could spur hair growth

Are we ushering into an era of no baldness?
Ameya Paleja
baldness.jpg
  • Hair follicles can regenerate without any injury.
  • TGF-beta can activate cell division and program cell death.
  • It is all about the levels of TGF-beta present.

A team of scientists at the University of California, Riverside (UCR) have zeroed in on the single chemical that is key to hair growth and fall, an organizational press release said.

Hair is a fascinating subject for scientific study. It has a root system that nourishes every strand while it is at the skin's surface. However, as the strand grows out of the system, the cells inside are very much dead, requiring no more nourishment and pushing outwards as more dead cells join at the base.

In most animals, hair growth and fall are coordinated with the change in seasons and handled together with quite some ease over time. So, it does seem odd that humans do not have very good control over their limited hairlines that seem to give way after reaching a certain age. Researchers have tried to understand the factors that influence hair loss and what could be done to arrest it.

The answer seems simple, stem cells.

How are stem cells involved in hair growth?

It might seem like scientists these days are trying to solve all problems with stem cells. However, in the case of hair, the problem appears to have 'stemmed' from them, anyways.

Below the root of each hair strand lies a follicle that nourishes the hair cells while they grow. The follicle is also home to a lot of stem cells, which it can quickly direct to carry out certain tasks.

In the human body, stem cells spring into action as a response to an injury; however, research studies have shown that stem cells work inside hair follicles, even in the absence of an injury.

Qixuan Wang, a mathematical biologist at UCR, and his team set out to discover how this works and arrived at a simple answer, TGF-beta.

How does TGF-beta control hair fall?

Transforming growth factor (TGF) beta is a type of small protein that works from outside the cells and is involved in cell signaling. Interestingly, TGF-beta is the sole chemical involved in both the activation of cell division inside the hair follicles as well as bringing it to an end.

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As with most chemicals in the human body, it is the amount of the chemical that makes the difference. In controlled quantities, TGF-beta activates cell division. When made in excess, it programs the cells to die.

Researchers are not really sure why the protein kills the hair follicle; however, it does not kill the stem cell reservoir inside the follicles. "When the surviving stem cells receive the signal to regenerate, they divide, make new cells, and develop into a new follicle," Wang said in the press release.

The researchers still need to determine how exactly TGF-beta activates cell division to be able to activate follicular stem cells and stimulate hair growth. Not only could this help cure baldness, but it could also help in the perfect healing, where hair begins to grow after a wound is healed.

The research findings were published in the Biophysical Journal.

Abstract

Hair follicles (HFs) are mini skin organs that undergo cyclic growth. Various signals regulate HF cell fate decisions jointly. Recent experimental results suggest that transforming growth factor beta (TGF-β) exhibits a dual role in HF cell fate regulation that can be either anti- or pro-apoptosis. To understand the underlying mechanisms of HF cell fate control, we develop a novel probabilistic Boolean network (pBN) model on the HF epithelial cell gene regulation dynamics. First, the model is derived from literature, then refined using single-cell RNA sequencing data. Using the model, we both explore the mechanisms underlying HF cell fate decisions and make predictions that could potentially guide future experiments: 1) we propose that a threshold-like switch in the TGF-β strength may necessitate the dual roles of TGF-β in either activating apoptosis or cell proliferation, in cooperation with bone morphogenetic protein (BMP) and tumor necrosis factor (TNF) and at different stages of a follicle growth cycle; 2) our model shows concordance with the high-activator-low-inhibitor theory of anagen initiation; 3) we predict that TNF may be more effective in catagen initiation than TGF-β, and they may cooperate in a two-step fashion; 4) finally, predictions of gene knockout and overexpression reveal the roles in HF cell fate regulations of each gene. Attractor and motif analysis from the associated Boolean networks reveal the relations between the topological structure of the gene regulation network and the cell fate regulation mechanism. A discrete spatial model equipped with the pBN illustrates how TGF-β and TNF cooperate in initiating and driving the apoptosis wave during catagen.

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