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Near Infrared (NIr) Light Increases Expression of a Marker of Mitochondrial Function in the Mouse Vestibular Sensory Epithelium
Published on: March 14, 2015
Cellular response to infrared radiation involves retrograde mitochondrial signaling
Peter Schroeder1, Corinna Pohl, Christian Calles
1Institut für Umweltmedizinische Forschung at the Heinrich-Heine-University Düsseldorf gGmbH, Auf'm Hennekamp 50, D-40225 Duesseldorf, Germany.
Free Radical Biology & Medicine
|June 15, 2007
Summary
Infrared A radiation (IRA) triggers gene expression in skin via mitochondrial reactive oxygen species (ROS) production. This retrograde signaling pathway differs from ultraviolet (UV) radiation responses.
Area of Science:
- Dermatology
- Molecular Biology
- Biochemistry
Background:
- Infrared A radiation (IRA) is a significant part of sunlight, known to induce gene transcription.
- The cellular response to IRA is less understood compared to ultraviolet (UV) radiation.
- Matrix metalloproteinase-1 (MMP-1) is a key gene involved in skin responses to radiation.
Purpose of the Study:
- To investigate the molecular mechanisms underlying IRA-induced gene expression in human skin.
- To determine the role of reactive oxygen species (ROS) and mitochondria in the IRA response.
- To compare the signaling pathways of IRA with those of UVB and UVA1 radiation.
Main Methods:
- Assessing IRA-induced MMP-1 expression in human skin fibroblasts.
- Utilizing MitoSox staining to detect mitochondrial superoxide anion production.
- Employing the mitochondrial-targeted antioxidant MitoQ and chemical inhibitors of the electron transport chain.
- Experimenting with rho0 fibroblasts (lacking mitochondrial DNA) and PGC-1 overexpressing fibroblasts.
Main Results:
- IRA-induced MMP-1 expression is mediated by intracellular ROS formation.
- Mitochondrial superoxide anion production increased upon IRA irradiation.
- MitoQ treatment completely blocked IRA-induced responses, but not UVB or UVA1.
- Inhibition of the electron transport chain and the use of rho0 fibroblasts confirmed the mitochondrial origin of ROS in the IRA response.
- Fibroblasts overexpressing PGC-1 showed hypersensitivity to IRA, indicating enhanced mitochondrial activity.
Conclusions:
- IRA elicits a distinct retrograde signaling response in human skin, originating from the mitochondrial electron transport chain.
- This mitochondrial ROS-dependent pathway for IRA differs significantly from the mechanisms activated by UVB and UVA1 radiation.
- Understanding this IRA-specific pathway is crucial for developing targeted photoprotective strategies.
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