Summary: The researchers discovered how the TGF-beta protein controls the process by which hair follicles, including stem cells, divide and generate new cells or undergo apoptosis. The research may offer new treatment options for baldness and therapies for wound healing.
A source: UCR
Only one chemical is important for controlling when hair follicle cells divide and when they die. This discovery not only cures baldness but also accelerates wound healing, as follicles are a source of stem cells.
Most cells in the human body have a specific shape and function that is determined during embryonic development and does not change. For example, a blood cell cannot become a nerve cell or vice versa. Stem cells are like empty tiles in a game of Scrabble; they can transform into other types of cells.
Their adaptability makes them useful for repairing damaged tissues or organs.
“In science fiction, when characters heal quickly from injuries, the idea is that stem cells allow this,” said Qisuan Wang, a mathematical biologist at UC Riverside and one of the study’s authors.
“In real life, our new research brings us closer to understanding cell behavior so we can control it and heal wounds,” Wang said. This study has recently been presented in detail Journal of Biophysics an article.
The liver and stomach repair themselves in response to injury. But Wang’s team studied hair follicles because they are the only human organ that can renew itself automatically and periodically, even without injury.
Scientists have discovered how a type of protein, TGF-beta, controls the process by which cells in hair follicles, including stem cells, divide and make new cells, or cause them to die, eventually leading to the death of the entire hair follicle.
“TGF-beta has two opposing roles. It activates some hair follicle cells to generate new life and then helps organize apoptosis, the process of cell death,” Wang said.
As with many chemicals, it’s the amount that makes the difference. If a cell produces a certain amount of TGF-beta, it activates cell division. Too much of it causes apoptosis.
No one knows exactly why follicles kill themselves. Some hypotheses suggest that this is an inherited trait from animals that shed their fur to cope with the hot summer temperatures, or in an attempt to camouflage themselves.
“Although the hair follicle kills itself, it never kills the stem cell reservoir. “When the surviving stem cells receive a signal to regenerate, they divide and generate a new cell and become a new follicle,” Wang said.
If scientists can pinpoint the way TGF-beta activates cell division and how the chemical interacts with other important genes, it may be possible to activate follicle stem cells and stimulate hair growth.
Since many animals, including humans, have hairy skin, complete wound healing requires renewal of hair follicles. Being able to precisely control TGF-beta levels could also one day cure the baldness that plagues millions of people around the world.
“Potentially, our work can offer something to help people suffering from a variety of problems,” Wang said.
This is news about baldness and genetics research
Author: Jules Bernstein
A source: UCR
The connection: Jules Bernstein – UCR
Photo: Photo courtesy of Helpaeatcontu
Original research: Closed access.
Qixuan Wang et al. Journal of Biophysics
A probabilistic logic model for the regulation of hair follicle cell fate by TGF-β
Hair follicles (HFs) are mini skin organs that undergo cyclical growth. Different signals cooperatively regulate HF cell fate decision. Recent experimental results indicate a dual role of transforming growth factor beta (TGF-ββ) in the regulation of HF cell fate, which can be either anti-apoptotic or pro-apoptotic.
To understand the underlying mechanisms of HF cell fate control, we develop a novel probabilistic logic network (pBN) model of HF epithelial cell gene regulatory dynamics. First, the model was derived from the literature and then refined using single-cell RNA sequencing data.
Using the model, we both explore the mechanisms underlying HF cell fate decisions and make predictions to guide future experiments: 1) We propose that threshold-like switching of TGF-ββ potency may require a dual role for TGF-ββ. in association with bone morphogenetic protein (BMP) and tumor necrosis factor (TNF) and activation of apoptosis or cell proliferation at different stages of the follicle growth cycle; 2) our model shows agreement with the high-activator-low-inhibitor theory of anagen initiation; 3) we assume that TNF may be more effective in initiating catagen than TGF-ββ, and they may cooperate in a two-step fashion; 4) finally, gene knockout and overexpression predictions reveal the role of each gene in regulating HF cell fate.
Attractor and motif analysis from connected Boolean networks reveals connections between the topological structure of the gene regulatory network and the mechanism of cell fate regulation.
A discrete spatial model fitted with pBN shows how TGF-ββ and TNF cooperate to initiate and drive the wave of apoptosis during catagen.