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Changes in expression of apoptosis-associated genes in skin mark early catagen
M Seiberg1, J Marthinuss, K S Stenn
1Skin Biology Research Center, R.W. Johnson Pharmaceutical Research Institute, Raritan, NJ 08869-0602.
Abstract:
Programmed cell death is central to hair biology, as the hair follicle undergoes cycles of growth (anagen), regression (catagen), and rest (telogen). During catagen, the hair follicle shortens via a pathway of programmed cell death and apoptosis. The molecular mechanisms involved in this process have not been elucidated yet. Using reverse transcriptase-polymerase chain reaction, we examined in this study the expression in total skin, throughout one hair cycle, of a series of regulatory genes associated with apoptosis. We show that gene expression within skin is hair-cycle-dependent. Transforming growth factor-beta was expressed immediately before catagen; therefore, it might be involved in the early signaling of this process. Tumor necrosis factor-beta was expressed during catagen and might be involved in follicular apoptosis. Several proto-oncogenes and transcription factors have been described in the regulation of apoptosis in other systems. Here we show that the transcript levels of c-myc, c-myb, and c-jun changed immediately before or during early catagen and thus could be involved in the signaling or regulation of catagen. Levels of p53 remained constant throughout anagen and catagen, suggesting that p53 is not involved in the developmentally induced apoptosis of the hair follicle. The variable expression throughout the hair cycle of the genes described demonstrates the dynamic changes of the skin and underscores the importance of studying the complete hair cycle when characterizing any molecule in skin.
Insights
Programmed cell death drives hair follicle cycling. Key genes like transforming growth factor-beta and tumor necrosis factor-beta show hair-cycle-dependent expression, regulating apoptosis during catagen.
Area of Science:
- Hair biology and follicle cycle dynamics.
- Molecular mechanisms of programmed cell death (apoptosis).
- Gene expression regulation during skin cycling.
Background:
- Hair follicles undergo cyclical phases: anagen (growth), catagen (regression), and telogen (rest).
- Programmed cell death and apoptosis are critical for hair follicle regression during the catagen phase.
- The precise molecular regulators of hair follicle apoptosis remain largely uncharacterized.
Purpose of the Study:
- To investigate the expression patterns of apoptosis-related regulatory genes during the hair cycle.
- To identify molecular signals involved in the programmed cell death of the hair follicle during catagen.
- To determine the role of specific genes, including proto-oncogenes and transcription factors, in hair follicle apoptosis.
Main Methods:
- Analysis of gene expression in total skin throughout a complete hair cycle.
- Utilized reverse transcriptase-polymerase chain reaction (RT-PCR) to quantify transcript levels.
- Examined a series of regulatory genes associated with apoptosis.
Main Results:
- Gene expression in the skin is significantly dependent on the hair cycle stage.
- Transforming growth factor-beta expression precedes catagen, suggesting early signaling involvement.
- Tumor necrosis factor-beta expression occurs during catagen, implicating it in follicular apoptosis.
- Transcript levels of c-myc, c-myb, and c-jun change around early catagen, indicating roles in regulation.
- p53 expression remained constant, suggesting it is not involved in developmentally induced hair follicle apoptosis.
Conclusions:
- Hair follicle apoptosis during catagen is regulated by a dynamic and hair-cycle-dependent gene expression program.
- Transforming growth factor-beta, tumor necrosis factor-beta, c-myc, c-myb, and c-jun are potentially key players in hair follicle regression.
- The study highlights the necessity of examining gene expression across the entire hair cycle for accurate molecular characterization in skin.
- p53 does not appear to play a role in the developmentally regulated apoptosis of the hair follicle.