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Updated: Dec 1, 2025
A New Technique for Quantitative Analysis of Hair Loss in Mice Using Grayscale Analysis
Published on: March 9, 2015
Hair graying with aging in mice carrying oncogenic RET
Machiko Iida1,2, Akira Tazaki1, Ichiro Yajima1,2
1Department of Occupational and Environmental Health, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Abstract:
Hair graying is a representative sign of aging in animals and humans. However, the mechanism for hair graying with aging remains largely unknown. In this study, we found that the microscopic appearance of hair follicles without melanocyte stem cells (MSCs) and descendant melanocytes as well as macroscopic appearances of hair graying in RET-transgenic mice carrying RET oncogene (RET-mice) are in accordance with previously reported results for hair graying in humans. Therefore, RET-mice could be a novel model mouse line for age-related hair graying. We further showed hair graying with aging in RET-mice associated with RET-mediated acceleration of hair cycles, increase of senescent follicular keratinocyte stem cells (KSCs), and decreased expression levels of endothelin-1 (ET-1) in bulges, decreased endothelin receptor B (Ednrb) expression in MSCs, resulting in a decreased number of follicular MSCs. We then showed that hair graying in RET-mice was accelerated by congenitally decreased Ednrb expression in MSCs in heterozygously Ednrb-deleted RET-mice [Ednrb(+/-);RET-mice]. We finally partially confirmed common mechanisms of hair graying with aging in mice and humans. Taken together, our results suggest that age-related dysfunction between ET-1 in follicular KSCs and endothelin receptor B (Ednrb) in follicular MSCs via cumulative hair cycles is correlated with hair graying with aging.
Insights
New research reveals that aging hair follicles lose melanocyte stem cells, leading to gray hair. This study identifies a key molecular pathway involving endothelin-1 and its receptor, offering insights into age-related hair graying.
Area of Science:
- Cell Biology
- Dermatology
- Aging Research
Background:
- Hair graying is a visible indicator of aging in humans and animals.
- The precise biological mechanisms underlying age-related hair graying are not fully understood.
- Previous studies have noted similarities in hair graying between humans and certain mouse models.
Purpose of the Study:
- To investigate the mechanisms of age-related hair graying using a novel mouse model.
- To identify molecular factors contributing to the loss of melanocytes in aging hair follicles.
- To explore potential common pathways for hair graying in mice and humans.
Main Methods:
- Utilized RET-transgenic mice (RET-mice) exhibiting hair graying.
- Examined hair follicle histology, focusing on melanocyte stem cells (MSCs) and melanocytes.
- Analyzed gene expression of endothelin-1 (ET-1) and endothelin receptor B (Ednrb) in hair follicles.
- Investigated the impact of Ednrb deficiency on hair graying in RET-mice.
Main Results:
- RET-mice displayed hair graying consistent with human aging, characterized by a lack of MSCs and melanocytes.
- Hair graying in RET-mice correlated with accelerated hair cycles, increased senescent keratinocyte stem cells (KSCs), and reduced ET-1 and Ednrb expression.
- Decreased Ednrb expression in MSCs exacerbated hair graying in RET-mice.
- Identified a potential age-related dysfunction between ET-1 in KSCs and Ednrb in MSCs.
Conclusions:
- RET-mice serve as a valuable model for studying age-related hair graying.
- The study suggests a correlation between cumulative hair cycles and age-related hair graying.
- Dysfunctional interaction between ET-1 and Ednrb signaling pathways contributes to hair graying with aging.
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