Microvesicle Particle Cell Signaling Following Acute Cold Injury to Keratinocytes
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Authors
Richardsen, Philip G.
Issue Date
2025-12
Volume
10
Issue
Type
Journal Article
Language
Keywords
Alternative Title
Abstract
Every year, millions globally suffer from cold injury including hypothermia, frostbite, and trench foot. Within the United States, the Department of the Air Force has the greatest United States Military presence in Arctic and subarctic regions with personnel at high risk for cold injury. Sequelae associated with frostbite include inflammation, ischemia, necrosis, and self-amputation. Previously, the Travers group has shown that the lipid mediator Platelet activating factor (PAF) was biosynthesized and released by cells undergoing cold injury. Moreover, many environmental stressors which produce PAF also generate subcellular microvesicle particles (MVP). The goal for these studies was to define if cold injury results in MVP generation. Subsequent work has studied the involvement of PAF-Receptor (PAFR) and acid sphingomyelinase (aSMase) in the biosynthesis and release of MVP. Using the human keratinocyte-derived cell lines HaCaT, genetically engineered PAFR+ KBP and PAFR- KBM keratinocytes, as well as human ex vivo skin models, we find that cells undergoing Air Force relevant cold injury released MVPs consistent with the release of PAF in a PAFR-independent manner but with dependence on aSMase depending on injury condition, providing pharmacological targets to regulate the post-col injury nanoparticle cell-signaling response.
Description
Citation
Publisher
Creighton University
License
This material is copyrighted