Dermal sheath contraction powers stem cell niche relocation during hair cycle regression.

Science. 2019 Dec 19. pii: eaax9131. doi: 10.1126/science.aax9131. [Epub ahead of print]
Dermal sheath contraction powers stem cell niche relocation during hair cycle regression.
Heitman N1,2,3, Sennett R1,2,3, Mok KW1,2, Saxena N1,2,3, Srivastava D1,2, Martino P1,2, Grisanti L1,2, Wang Z4, Ma'ayan A4, Rompolas P5, Rendl M6,2,7.
Author information
1
Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
2
Department of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
3
Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
4
Department of Pharmacological Sciences, Mount Sinai Center for Bioinformatics, BD2K-LINCS Data Coordination and Integration Center, Knowledge Management Center for Illuminating the Druggable Genome (KMC-IDG), Icahn School of Medicine at Mount Sinai, New York, NY, USA.
5
Department of Dermatology, Institute for Regenerative Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
6
Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. michael.rendl@mssm.edu.
7
Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Tissue homeostasis requires the balance of growth by cell production and regression through cell loss. In the hair cycle during follicle regression, the niche traverses the skin through an unknown mechanism to reach the stem cell reservoir and trigger new growth. Here we identify the dermal sheath that lines the follicle as the key driver of tissue regression and niche relocation via the smooth muscle contractile machinery that generates centripetal constriction force. We reveal that the calcium/calmodulin/myosin light chain kinase pathway controls sheath contraction. When this pathway is blocked, sheath contraction is inhibited, impeding follicle regression and niche relocation. Thus, our study identifies the dermal sheath as smooth muscle that drives follicle regression for reuniting niche and stem cells in order to regenerate tissue structure during homeostasis

+1 for the scalp tension theory?

Rudiger wrote:+1 for the scalp tension theory?

CS is this mostly what the study is saying?

There is a normal contraction of the dermal sheath that surrounds the hair follicle.

If this contraction no longer functions, hair follicle regression will occur.

Here's a paper on biological cell division process of centripetal constriction force that is normal for this process.

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0069750

So what controls this contraction?

Calmodulin (CaM)-dependent myosin light chain kinase (MLCK) controls this smooth muscle contraction of the dermal sheath.

Calmodulin (CaM) is a ubiquitous Ca2+-binding protein that regulates as many as 80 target proteins, many of which are enzymes whose activity is stimulated by CaM in a Ca2+-dependent manner. Or to put it another way. it binds to calcium, which when inflammation exists chronically, tends to attract calcium deposition.

Most forms of aging involve calcium deposition. I would presume that a calcium-channel blocker would be helpful. A natural one of course.