OR WAIT null SECS
Armand Butera is the assistant editor for HCPLive. He attended Fairleigh Dickinson University and graduated with a degree in communications with a concentration in journalism. Prior to graduating, Armand worked as the editor-in-chief of his college newspaper and a radio host for WFDU. He went on to work as a copywriter, freelancer, and human resources assistant before joining HCPLive. In his spare time, he enjoys reading, writing, traveling with his companion and spinning vinyl records. Email him at email@example.com.
Dr. Ezhkova and fellow investigators found that low UV exposure prompted an increase in pigmentation production through melanocytes in the body.
A recent study from Mount Sinai Medical Center found that ultraviolet (UV) light exposure led epigenetic changes in the epidermis of patients, resulting in skin pigmentation.
Though the public are exposed to UV light on a regular basis, excess exposure can be detrimental to the body and is often cited as 1 of the main causes of cancer.
To prevent DNA damage, epidermal cells become pigmented by melanocytes. However, prior to the study the molecular mechanisms between epidermal cells and melanocytes were not well understood.
In an interview with HCPLive, Elena Ezhkova, PhD, Professor of Cell, Professor of Cell, Developmental and Regenerative Biology and Dermatology, at Black Family Stem Cell Institute, Icahn School of Medicine, Mount Sinai, spoke of how the protective measures of epidermal cells lead to an increase in pigmentation production in melanocytes.
In current studies, UV treatments had been used, often in high doses, to treat patients with skin hypopigmentation conditions such as vitiligo.
Additionally, prior data suggested that high doses of UV radiation led to an activation of p53, a tumor suppressive gene, that in turn activated melanocytes that produced pigment and transferred to epidermal keratinocytes.
“We knew that we knew that epidermal keratinocytes and melanocytes talk to each other, (and) we knew that epidermal keratinocytes might be the first cell type of the skin that receive UV, that that are exposed to UV,” Ezhkova said. “So, they might be the first cell that senses UV. But what was unknown is how does it occur at physiological levels of UV exposure?”
During the study, an important distinction was made regarding transcriptional changes that occurred in high and low UV exposure.
“We identified this transcription sensor in case of high UV damage as p53,” Ezhkova sais. “In the case of low UV exposure, it is grommeted regulator complex called Polycomb complex, and in our case was showed that the levels and activity of this complex decreases upon UV exposure.”
Ezhkova and investigators found that the expression of key units within the Polycomb complex, combined with the levels of Polycomb-mediated repressive histone marks, decreased in the epidermis upon exposure.
Additionally, they identified an ECM protein, COL2A1, as a critical regulator of melanocyte melanogenesis, though the mechanism of how the protein interacts with melanocytes to transfer to epidermal keratinocytes was still unknown.
“The cells have this intrinsic high potential for mobility, so changes in the extracellular matrix of the skin then sort of attract or trap melanocytes there and then they produce pigment and deposit to the cells of epidermis,” Ezhkova said. “So, this is something that we need to investigate in the future molecular mechanisms of how exactly COL2A1 stimulates melanocytes to produce pigment.”
To hear more about Dr. Ezhkova’s recent study, and the future of UV exposure studies in relation to the epidermis, watch the interview above.