Radioisotope Research Laboratory

Japanese

Ultraviolet rays in sunlight cause short- or long-term damage to the skin depending on the wavelength of UV light and how it is exposed, and induce diseases depending on the degree of damage and damage accumulation.
Our laboratory aims to elucidate the mechanisms of the phenomena and responses (cellular responses) that occur in cells exposed to ultraviolet rays, and to develop research that will be useful for the mitigation and treatment of skin disorders and diseases caused by ultraviolet rays.

Research Content

Involvement of TRP channels in the cellular response to UVA irradiation

< Cell membrane proteins (receptors / ion channels) respond to UVA? >
TRP channels are cation channels that are activated by various stimuli such as temperature changes, mechanical stimuli, osmotic changes, pain, pH changes, and oxidative stress, and function as sensor proteins in cells.
Since UV exposure has been reported to activate TRP channels via G protein-coupled receptors, we are investigating how TRP channel activation is related to the prduction of inflammatory substances that contribute to skin disorder.

Involvement of ATP signaling in the cellular response to UVA irradiation

A) searching for a novel mechanism of photoaging by targeting ATP and its receptors
< Is ATP signaling involved in skin photoaging? >
Photoaging is the aging of the skin caused by long-term exposure to ultraviolet rays (especially UVA). The mechanisms underlying the onset and progression of photoaging are complex.
We are searching for new mechanisms of photoaging in order to find factors that regulate photoaging.
As a result, we found that UVA exposure causes release of ATP to the extracellular space through several channels and receptors on the cell membrane, activates P2 receptors, and induces the production of inflammatory cytokines.

B) Involvement of ATP signaling in the mechanism of DNA damage induced by UVA irradiation
< Is ATP involved in UVA-induced DNA damage? >
Skin contains various types of cells such as keratinocytes, fibroblasts, mast cells, and Langerhans cells, etc.
Since UVA reaches deeper into the skin than UVB, it may affect blood cells in capillaries.
UVA rarely damages DNA directly, because it is not readily absorbed by DNA, but can cause indirect damage through ROS production.
Since the sensitivity of cells in skin to UVA is thought to vary depending on the cell type, we are investigating the involvement of ATP signaling in UVA-induced DNA damage and subsequent cellular responses, such as repair and cell death, using model cells of various types in skin.