> Researchers at the University of California, Riverside, found that a sole chemical[, TGF-beta, ]is responsible for hair follicles dividing and dying[: such chemical] could «not only treat baldness, but ultimately speed wound healing»

> «Even when a hair follicle kills itself, it never kills its stem cell reservoir. When the surviving stem cells receive the signal to regenerate, they divide, make new cell and develop into a new follicle»

--

Original press release from Uni Cal-Riverside:

https://news.ucr.edu/articles/2022/07/25/chemical-controllin...

> [Qixuan Wang, mathematical biologist and study co-author: ]«our new research gets us closer to understanding stem cell behavior, so that we can control it and promote wound healing»

> The liver and stomach regenerate themselves in response to wounds. However, Wang’s team studied hair follicles because they’re the only organ in humans that regenerates automatically and periodically, even without injury

> As with many chemicals, it is the amount that makes the difference. If the cell produces a certain quantity of TGF-beta, it activates cell division. Too much of it causes apoptosis

> If scientists can determine more precisely the way TGF-beta activates cell division, and how the chemical communicates with other important genes, it might be possible to activate follicle stem cells and stimulate hair growth

--

Original research article:

A probabilistic Boolean model on hair follicle cell fate regulation by TGF-β - https://www.cell.com/biophysj/fulltext/S0006-3495(22)00428-3

> 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