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Stress-induced premature senescence of dermal papilla cells compromises hair follicle epithelial-mesenchymal interaction.

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Stress-induced premature senescence of dermal papilla cells compromises hair follicle epithelial-mesenchymal interaction.

Post  CausticSymmetry on Wed Feb 01, 2017 12:22 pm

J Dermatol Sci. 2017 Jan 5. pii: S0923-1811(17)30026-9. doi: 10.1016/j.jdermsci.2017.01.003. [Epub ahead of print]
Stress-induced premature senescence of dermal papilla cells compromises hair follicle epithelial-mesenchymal interaction.
Huang WY1, Huang YC1, Huang KS1, Chan CC2, Chiu HY3, Tsai RY4, Chan JY5, Lin SJ6.

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.

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Re: Stress-induced premature senescence of dermal papilla cells compromises hair follicle epithelial-mesenchymal interaction.

Post  cdto2012 on Wed Feb 01, 2017 6:32 pm

A note to consider, the stress referred to is free radical oxygen induced breakdown, via hydrogen peroxide. Although mental stress negatively effects the body, this was not the focus of the study.

Peroxides and oxygen are a healthy part of living tissue processes. The focus is how to properly protect the cells from being weak and vulnerable. Like ozone in the air, it is usually what the ozone is attached to and removing from the air that is the problem. These active oxygens will often react/attach to toxins(or kill viruses), so the chemistry needs to be well defined to understand the process .

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Re: Stress-induced premature senescence of dermal papilla cells compromises hair follicle epithelial-mesenchymal interaction.

Post  CausticSymmetry on Sat Feb 04, 2017 4:21 am

For me, the main take away is that interleukin-6 (this is known from previous research) is a cytokine that exacerbates hair loss. Marine oils, such as fish, cod, krill oil, etc will reduce these levels.


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Re: Stress-induced premature senescence of dermal papilla cells compromises hair follicle epithelial-mesenchymal interaction.

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