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Published on: April 14, 2010
Mitochondrial gene expression changes in cultured human skin cells following simulated sunlight irradiation
1Mitochondrial Biology & Radiation Research Centre, Dept. of Life Sciences, Institute of Technology Sligo, Ash Lane, Sligo, Ireland.
Background:
Exposure of skin to simulated sunlight irradiation (SSI) has being extensively researched and shown to be the main cause for changes in the skin including changes in cellular function and generation of reactive oxygen species (ROS). This oxidative stress can subsequently exert downstream effects and the subcellular compartments most affected by this oxidative stress are mitochondria. The importance of functional mitochondrial morphology is apparent as morphological defects are related to many human diseases including diabetes mellitus, liver disease, neurodegenerative diseases, aging and cancer.
Objective:
The main objective of this study was to evaluate solar radiation-induced changes in mitochondrial gene expression in human skin cells using a Q-Sun solar simulator to deliver a close match to the intensity of summer sunlight.
Methods:
Spontaneously immortalised human skin epidermal keratinocytes (HaCaT) and Human Dermal Fibroblasts (HDFn) were divided into two groups. Group A were irradiated once and Group B twice 7days apart; following irradiation, mitochondrial gene expression was evaluated 1, 4 and 7days post primary exposure for group A and 1, 4, 7 and 14days post-secondary exposure for group B.
Results:
Both the epidermal and dermal cells displayed significant reduced expression of the genes analysed for mitochondrial morphology and function; however, epidermal cells displayed this reduction post SSI earlier then dermal cells at multiple time points.
Conclusion:
The data presented here reinforces the fact that epidermal cells, while displaying a heightened sensitivity to sunlight, are less prone to changes in gene expression, while dermal cells, which appear to be more resilient are possibly more prone to genomic instability and mitochondrial damage.
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