iBet uBet web content aggregator. Adding the entire web to your favor.
iBet uBet web content aggregator. Adding the entire web to your favor.



Link to original content: http://pubmed.ncbi.nlm.nih.gov/35795256/
Regulation of signaling pathways in hair follicle stem cells - PubMed Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Jul 4:10:tkac022.
doi: 10.1093/burnst/tkac022. eCollection 2022.

Regulation of signaling pathways in hair follicle stem cells

Xiaoxiang Wang  1 , Yinghui Liu  2 , Jia He  1 , Jingru Wang  1 , Xiaodong Chen  1 , Ronghua Yang  1
Affiliations
Review

Regulation of signaling pathways in hair follicle stem cells

Xiaoxiang Wang et al. Burns Trauma. .

Abstract

Hair follicle stem cells (HFSCs) reside in the bulge region of the outer root sheath of the hair follicle. They are considered slow-cycling cells that are endowed with multilineage differentiation potential and superior proliferative capacity. The normal morphology and periodic growth of HFSCs play a significant role in normal skin functions, wound repair and skin regeneration. The HFSCs involved in these pathophysiological processes are regulated by a series of cell signal transduction pathways, such as lymphoid enhancer factor/T-cell factor, Wnt/β-catenin, transforming growth factor-β/bone morphogenetic protein, Notch and Hedgehog. The mechanisms of the interactions among these signaling pathways and their regulatory effects on HFSCs have been previously studied, but many mechanisms are still unclear. This article reviews the regulation of hair follicles, HFSCs and related signaling pathways, with the aims of summarizing previous research results, revealing the regulatory mechanisms of HFSC proliferation and differentiation and providing important references and new ideas for treating clinical diseases.

Keywords: Differentiation; Hair follicle stem cells; Proliferation; Regenerative; Repair; Signaling pathways.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Mechanism of Wnt/β-catenin signaling pathway. When the Wnt signal is inactivated, the destruction complex ubiquitinates β-catenin to degrade it, and then it is digested in the proteasome. When the Wnt signal is activated, the Wnt protein interacts with Frizzled receptors and lipoprotein receptor-related protein 5/6 (LRP5/6). Axis inhibition protein (Axin) binds to the tail of LRP5/6, and then Disheveled (Dsh) restores the activity of β-catenin by phosphorylating and inhibiting the activity of glycogen synthase kinase-3 (GSK3) so that β-catenin accumulates and enters the nucleus with lymphoid enhancer factor/T-cell factor (LEF/TCF) transcription factors to regulate target gene transcription. β-TrCP/SKP β-transducin repeat-containing protein/s-phase kinase-associated protein
Figure 2.
Figure 2.
Mechanism of transforming growth factor-β/bone morphogenetic protein (TGF-β/BMP) signaling pathway. The TGF-β/BMP ligand binds to the receptor to form a binary complex, while the type II receptor activates the type I receptor, which further phosphorylates the R-Smad protein so that it can bind to Co-Smad4, enter the nucleus and activate a series of downstream target genes
Figure 3.
Figure 3.
Mechanism of Notch signaling pathway. In the Golgi, the first cleavage (S1) occurs under the action of the furin-like converting enzyme. In the second lysis (S2), the extracellular region (NECD) is phagocytosed by the surface cells and then the intracellular region (NICD) is lysed for a third time under the action of γ-secretase and mutant presenilin (S3), after which it enters the nucleus, and initiates the transcription of downstream target genes. ML metal loprotease, TACE TNF-α-convertingenzyme, CSL CBF-1, Suppressor of hairless, Lag
Figure 4.
Figure 4.
Mechanism of hedgehog (HH) signaling pathway. When there is no HH, patched (PTCH) will inhibit the activity of smoothened (Smo), leading to the termination of transcription of downstream target gene. When SHH is present, PTCH binds to SHH, releasing Smo and allowing the glioma (Gli) protein and protein kinase A (PKA) to form a macromolecular complex, such that the full-length Gli protein enters the nucleus to initiate transcription of downstream target genes
Figure 5.
Figure 5.
Mechanism of PI3K/AKT signaling pathway. When the ligand and receptor bind, PI3K can be activated. Phosphoinositide 3-kinase (PIP3) produced on the plasma membrane binds phosphorylated Thr308 and Ser473 through PI3K-dependent kinase 1 (PDK1) and PI3K-dependent kinase 2 (PDK2), respectively, resulting in AKT (protein kinase B) activation and action on downstream molecules
Figure 6.
Figure 6.
The interactive networks of signaling pathways in hair follicle stem cells. LEF/TCF lymphoid enhancer factor/T-cell factor, BMP/TGF-β bone morphogenetic protein/transforming growth factor-β, HH hedgehog
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Paus R, Cotsarelis G. The biology of hair follicles. N Engl J Med. 1999;341:491–7. - PubMed
    1. Stenn KS, Paus R. Controls of hair follicle cycling. Physiol Rev. 2001;81:449–94. - PubMed
    1. Cotsarelis G, Sun TT, Lavker RM. Label-retaining cells reside in the bulge area of pilosebaceous unit: implications for follicular stem cells, hair cycle, and skin carcinogenesis. Cell. 1990;61:1329–37. - PubMed
    1. Nicu C, Wikramanayake TC, Paus R. Clues that mitochondria are involved in the hair cycle clock: MPZL3 regulates entry into and progression of murine hair follicle cycling. Exp Dermatol. 2020;29:1243–9. - PubMed
    1. Geyfman M, Plikus MV, Treffeisen E, Andersen B, Paus R. Resting no more: re-defining telogen, the maintenance stage of the hair growth cycle. Biol Rev Camb Philos Soc. 2015;90:1179–96. - PMC - PubMed