Stress-induced Premature Senescence Of Dpcs Compromises Hair Follicle Epithelial-mesenchymal Interac

[InBeforeTheCure]

Highlights

• •Prematurely senescent dermal papilla cells still preserve key dermal papilla signature gene expression.
• •They lose the ability to induce new hair follicles and, instead, promote epidermal differentiation while inhibiting follicular differentiation.
• •They produce more IL-6 that inhibits clonal keratinocyte growth in vitro and block telogen to anagen transition in vivo.
• •Premature mesenchymal aging in hair follicles can compromise the function and regeneration of hair follicles.

Abstract
Background

Hair follicle is miniorgan constituted by keratinocytes and its distinctive mesenchyme of dermal papilla. Its aging is characterized by organ atrophy and impaired stem cell activation and differentiation. The contribution of dermal papilla to hair follicle aging change is not well understood.

Objective
This work was aimed at exploring the possible role of premature dermal papilla senescence in the pathogenesis of hair follicle aging.

Methods
Dermal papilla cells were challenged with H2O2 to induce premature senescence and the proliferation, apoptosis, gene expression and protein secretion were characterized. Its effect on epithelial-mesenchymal interaction was analyzed by co-culture in vitro and implantation of protein-coated beads in vivo.

Result
Dermal papilla cells were more resistant to oxidative stress-induced apoptosis than dermal fibroblasts. The surviving dermal papilla cells showed signs of senescence but still preserved key dermal papilla signature gene expression. In addition to the failure to respond to mitogenic stimulation from keratinocytes, they lost the ability to induce hair follicle neogenesis, promoted interfollicular epidermal differentiation, inhibited follicular differentiation and, importantly, suppressed clonal growth of hair follicle stem cells. They produced higher levels of multiple inflammatory cytokines, including IL-6. Functionally, IL-6 inhibited clonal keratinocyte growth in vitro and blocked the transition from telogen to anagen in vivo.

Conclusion
Stress-induced premature dermal papilla senescence can contribute to hair follicle aging change due to compromised epithelial-mesenchymal interaction.

Link: http://www.jdsjournal.com/article/S0923-1811(17)30026-9/abstract

Full text manuscript attached.

 

[Giiizmo]

Dermal papilla cells were challenged with H2O2 to induce premature senescence and the proliferation, apoptosis, gene expression and protein secretion were characterized. Its effect on epithelial-mesenchymal interaction was analyzed by co-culture in vitro and implantation of protein-coated beads in vivo.

[...] The surviving dermal papilla cells showed signs of senescence but still preserved key dermal papilla signature gene expression. In addition to the failure to respond to mitogenic stimulation from keratinocytes, they lost the ability to induce hair follicle neogenesis, promoted interfollicular epidermal differentiation, inhibited follicular differentiation and, importantly, suppressed clonal growth of hair follicle stem cells. They produced higher levels of multiple inflammatory cytokines, including IL-6. Functionally, IL-6 inhibited clonal keratinocyte growth in vitro and blocked the transition from telogen to anagen in vivo.

Most forum users usually dismiss any notion that stress could be a factor in hair loss. Now can we start talking about stress-induced triggering / amplification of androgenetic alopecia?

It's somewhat comforting to know that the numerous anecdotal reports from Androgenetic Alopecia sufferers incriminating stress as playing a role in the disease could possibly be right. That means that preventative measures could be taken to diminish the effect of stress on our precious follicles.

Since the article directly addresses one of the most common reactive oxygen species, that is H2O2, wearing a hat when under the sun already sounds like a good idea and further validates a common advice given to hair loss sufferers.

However, during times of environmental stress (e.g., UV or heat exposure), ROS levels can increase dramatically.[2] This may result in significant damage to cell structures. Cumulatively, this is known as oxidative stress.