Related Experiment Video

Updated: Oct 7, 2026

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells
06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

p53 Involvement in the control of murine hair follicle regression

V A Botchkarev1, E A Komarova, F Siebenhaar

  • 1Department of Dermatology, Boston University School of Medicine, Boston, Massachusetts 02118, USA. vladbotc@bu.edu

The American Journal of Pathology
|June 8, 2001
PubMed

Insights

The tumor suppressor p53 (also known as TP53) plays a key role in hair follicle apoptosis during catagen. P53 knockout mice exhibit delayed catagen, suggesting its therapeutic potential for hair loss conditions.

Area of Science:

  • Molecular Biology
  • Dermatology
  • Cell Biology

Background:

  • p53 is a crucial transcription factor regulating cellular responses, including apoptosis.
  • While p53's role in radiation- and chemotherapy-induced hair follicle apoptosis is known, its function in physiological hair follicle regression (catagen) is unclear.

Purpose of the Study:

  • To investigate the role of p53 in the apoptosis-driven process of physiological hair follicle catagen.
  • To explore the potential of targeting p53 for managing hair growth disorders.

Main Methods:

  • Immunohistochemical analysis of p53 expression and apoptotic markers in hair follicles during catagen.
  • Comparison of catagen progression and apoptosis levels in wild-type and p53 knockout mice.
  • Analysis of p53 target gene expression (Bax, Bcl-2, IGFBP-3) in p53 null hair follicles.

Main Results:

  • p53 protein is highly expressed and co-localized with apoptotic markers in regressing hair follicle compartments.
  • p53 knockout mice displayed significantly delayed catagen and reduced hair matrix apoptosis.
  • p53 null hair follicles showed altered expression of key catagen regulatory genes, including Bax, Bcl-2, and IGFBP-3.

Conclusions:

  • p53 is integral to the control of apoptosis during physiological hair follicle regression.
  • p53 antagonists may offer a therapeutic strategy for hair loss disorders involving premature catagen, such as androgenetic alopecia, alopecia areata, and telogen effluvium.

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Multipotency and Niche of Bulge Stem Cell01:06

Multipotency and Niche of Bulge Stem Cell

A hair follicle or HF is a small part of the skin that produces the hair shaft. Paul Gerson Unna was the first to observe a bulge in the human hair follicle's outer root sheath (ORS). The bulge is present between the sebaceous gland and the arrector pili muscle and is the niche for hair follicle stem cells (HFSCs). The bulge is also a niche for melanocyte stem cells, and their loss results in graying of hair. The HFSCs express Sox9 and Lhx2, which help them maintain stemness and prevent...
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...