Hair Follicle Stem Cells and Hair Regeneration

Author(s):  
Sung-Jan Lin ◽  
Wen-Yen Huang ◽  
Chih-Chiang Chen ◽  
Mingxing Lei ◽  
Jin-Bon Hong
2020 ◽  
pp. 265-296
Author(s):  
Sung-Jan Lin ◽  
Wen-Yen Huang ◽  
Chih-Chiang Chen ◽  
Mingxing Lei ◽  
Jin-Bon Hong

2016 ◽  
Author(s):  
Yan Tang ◽  
Binping Luo ◽  
Zhili Deng ◽  
Ben Wang ◽  
Fangfen L Liu ◽  
...  

Background. Emerging researches revealed the essential role of mitochondria in regulating stem/progenitor cell differentiation of neural progenitor cells, mesenchymal stem cells and other stem cells through reactive oxygen species (ROS), Notch or other signaling pathway. And inhibition of mitochondrial synthesis protein resulted in extension of hair loss upon injury. However, alteration of mitochondrial morphology and metabolic function during hair follicle stem cells (HFSCs) differentiation and how it affects hair regeneration has not been elaborated. Methods. We compared the difference between telogen bulge cells and anagen matrix cells in mitochondrial morphology and activity. Expression levels of mitochondrial ROS and superoxide dismutase 2 (SOD2) were measured for evaluating redox balance. Besides, pyruvate dehydrogenase kinase (PDK) and pyruvate dehydrogenase (PDH) were detected to present the change in energetic metabolism during differentiation. To explore the effect of the mitochondrial metabolism on regulating hair regeneration, hair growth was observed after application of a mitochondrial respiratory inhibitor upon hair plucking. Results. During HFSCs differentiation, mitochondria became elongated with more abundant organized cristae and showed higher activity in differentiated cells. SOD2 was enhanced for redox balance with relatively poised ROS expression levels in differentiated cells. PDK increased in HFSCs while differentiated cells showed enhanced PDH, indicating that respiration converted from glycolysis to oxidative phosphorylation during differentiation. Inhibiting mitochondrial respiration in differentiated hair follicle cells upon hair plucking held back hair regeneration in vivo. Conclusions. Upon HFSCs differentiation, mitochondria was elongated with more abundant cristae and showed higher activity, accompanied with activated aerobic respiration in differentiated cells for higher energy supply. And dysfunction of mitochondrial respiration delays hair regeneration upon injury.


PLoS Genetics ◽  
2021 ◽  
Vol 17 (12) ◽  
pp. e1009948
Author(s):  
Pooja Flora ◽  
Meng-Yen Li ◽  
Phillip M. Galbo ◽  
Maider Astorkia ◽  
Deyou Zheng ◽  
...  

Hair follicle stem cells (HFSCs) are multipotent cells that cycle through quiescence and activation to continuously fuel the production of hair follicles. Prior genome mapping studies had shown that tri-methylation of histone H3 at lysine 27 (H3K27me3), the chromatin mark mediated by Polycomb Repressive Complex 2 (PRC2), is dynamic between quiescent and activated HFSCs, suggesting that transcriptional changes associated with H3K27me3 might be critical for proper HFSC function. However, functional in vivo studies elucidating the role of PRC2 in adult HFSCs are lacking. In this study, by using in vivo loss-of-function studies we show that, surprisingly, PRC2 plays a non-instructive role in adult HFSCs and loss of PRC2 in HFSCs does not lead to loss of HFSC quiescence or changes in cell identity. Interestingly, RNA-seq and immunofluorescence analyses of PRC2-null quiescent HFSCs revealed upregulation of genes associated with activated state of HFSCs. Altogether, our findings show that transcriptional program under PRC2 regulation is dispensable for maintaining HFSC quiescence and hair regeneration.


2020 ◽  
Author(s):  
Rajiv L Tiwari ◽  
Pratibha Mishra ◽  
Nicola Martin ◽  
Nikhil Oommen George ◽  
Vadim Sakk ◽  
...  

SummaryNormal hair growth occurs in cycles, comprising growth (anagen), cessation (catagen) and rest (telogen). Upon aging, the initiation of anagen is significantly delayed, which results in impaired hair regeneration. Hair regeneration is driven by hair follicle stem cells (HFSCs). We show here that aged HFSCs present with a decrease in canonical Wnt signaling and a shift towards non-canonical Wnt5a driven signaling which antagonizes canonical Wnt signaling. Elevated expression of Wnt5a in HFSCs upon aging results in elevated activity of the small RhoGTPase Cdc42 as well as a change in the spatial distribution of Cdc42 within HFSCs. Treatment of aged HFSC with a specific pharmacological inhibitor of Cdc42 activity termed CASIN to suppress the aging-associated elevated activity of Cdc42 restored canonical Wnt signaling in aged HFSCs. Treatment of aged mice in vivo with CASIN induced anagen onset and increased the percentage of anagen skin areas. Aging-associated functional deficits of HFSCs are at least in part intrinsic to HFSCs and can be restored by rational pharmacological approaches.


2020 ◽  
Author(s):  
Rajiv Tiwari ◽  
Pratibha Mishra ◽  
Nicola Martin ◽  
Nikhil George ◽  
Vadim Sakk ◽  
...  

Abstract Normal hair growth occurs in cycles, comprising growth (anagen), cessation (catagen) and rest (telogen). Upon aging, the initiation of anagen is significantly delayed, which results in impaired hair regeneration. Hair regeneration is driven by hair follicle stem cells (HFSCs). We show here that aged HFSCs present with a decrease in canonical Wnt signaling and a shift towards non-canonical Wnt5a driven signaling which antagonizes canonical Wnt signaling. Elevated expression of Wnt5a in HFSCs upon aging results in elevated activity of the small RhoGTPase Cdc42 as well as a change in the spatial distribution of Cdc42 within HFSCs. Treatment of aged HFSC with a specific pharmacological inhibitor of Cdc42 activity termed CASIN to suppress the aging-associated elevated activity of Cdc42 restored canonical Wnt signaling in aged HFSCs. Treatment of aged mice in vivo with CASIN induced anagen onset and increased the percentage of anagen skin areas. Aging-associated functional deficits of HFSCs are at least in part intrinsic to HFSCs and can be restored by rational pharmacological approaches.


2016 ◽  
Author(s):  
Yan Tang ◽  
Binping Luo ◽  
Zhili Deng ◽  
Ben Wang ◽  
Fangfen L Liu ◽  
...  

Background. Emerging researches revealed the essential role of mitochondria in regulating stem/progenitor cell differentiation of neural progenitor cells, mesenchymal stem cells and other stem cells through reactive oxygen species (ROS), Notch or other signaling pathway. And inhibition of mitochondrial synthesis protein resulted in extension of hair loss upon injury. However, alteration of mitochondrial morphology and metabolic function during hair follicle stem cells (HFSCs) differentiation and how it affects hair regeneration has not been elaborated. Methods. We compared the difference between telogen bulge cells and anagen matrix cells in mitochondrial morphology and activity. Expression levels of mitochondrial ROS and superoxide dismutase 2 (SOD2) were measured for evaluating redox balance. Besides, pyruvate dehydrogenase kinase (PDK) and pyruvate dehydrogenase (PDH) were detected to present the change in energetic metabolism during differentiation. To explore the effect of the mitochondrial metabolism on regulating hair regeneration, hair growth was observed after application of a mitochondrial respiratory inhibitor upon hair plucking. Results. During HFSCs differentiation, mitochondria became elongated with more abundant organized cristae and showed higher activity in differentiated cells. SOD2 was enhanced for redox balance with relatively poised ROS expression levels in differentiated cells. PDK increased in HFSCs while differentiated cells showed enhanced PDH, indicating that respiration converted from glycolysis to oxidative phosphorylation during differentiation. Inhibiting mitochondrial respiration in differentiated hair follicle cells upon hair plucking held back hair regeneration in vivo. Conclusions. Upon HFSCs differentiation, mitochondria was elongated with more abundant cristae and showed higher activity, accompanied with activated aerobic respiration in differentiated cells for higher energy supply. And dysfunction of mitochondrial respiration delays hair regeneration upon injury.


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