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Ultraviolet B radiation generates platelet-activating factor-like phospholipids underlying cutaneous damage
Gopal K Marathe1, Christopher Johnson, Steven D Billings
1Human Molecular Biology and Genetics Program, University of Utah, Salt Lake City 84112-5330, USA. marathg@ccf.org
The Journal of Biological Chemistry
|August 24, 2005
Summary
Ultraviolet B (UVB) light triggers skin cell death by creating platelet-activating factor (PAF) analogs from phospholipids. These PAF analogs activate the PAF receptor, leading to inflammation and apoptosis in skin.
Area of Science:
- Dermatology
- Molecular Biology
- Biochemistry
Background:
- Ultraviolet B (UVB) radiation induces skin inflammation and cell death.
- The specific agents mediating UVB-induced cutaneous effects remain largely undefined.
- Platelet-activating factor (PAF) signaling is a key pathway in inflammatory responses.
Purpose of the Study:
- To investigate the role of the platelet-activating factor (PAF) signaling system in UVB-induced skin damage.
- To elucidate the mechanism by which UVB light activates the PAF receptor.
- To determine if PAF signaling contributes to UVB-mediated apoptosis in keratinocytes.
Main Methods:
- Utilized epidermoid cell lines and primary human keratinocytes.
- Overexpressed the PAF receptor in cells and an in vivo model (keratinocytes on SCID mice).
- Employed mass spectrometry to identify UVB-induced phospholipids and PAF analogs.
- Irradiated precursor phospholipids directly to assess fragmentation.
Main Results:
- Expression of the PAF receptor augmented UVB-induced apoptosis in both cell lines and in vivo.
- UVB irradiation of epidermal cells generated C4 PAF analogs and native PAF.
- Supplementation with 1-hexadecyl-2-arachidonoyl-sn-glycero-3-phosphocholine (HAPC) increased C4 PAF analog recovery post-UVB.
- Direct irradiation of HAPC resulted in fragmentation to C4-PAF receptor ligands, independent of photosensitizers.
Conclusions:
- UVB light photo-oxidizes cellular phospholipids, generating PAF analogs.
- These PAF analogs activate the PAF receptor, initiating a signaling cascade that promotes further PAF synthesis and apoptosis.
- PAF signaling is implicated in the cutaneous inflammation associated with photo-aggravated dermatoses.
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