Abstract:
:Ultra-violet B (UVB)-induced oxidative stress crucially perturbs the epidermal homeostasis, and the skin is endowed with protective mechanisms to take action against such damage. Here, we show the possible involvement of t-SNARE protein syntaxin3, a membrane fusion mediator of cytoplasmic vesicles, and which is released from dying keratinocytes, to play a role in this response. UVB irradiation, which generates reactive oxidative stress in cells, was shown to lead to the keratinocyte cell death accompanied by a release of cytoplasmic syntaxin3. We found that such extracellularly sourced syntaxin3 completely blocked the processing of a crucial effector for apoptotic cell death, caspase-3, and thus facilitated the survival of keratinocytes damaged by oxidative stress. These results demonstrate the latent prosurvival function of syntaxin3 and underline the importance of intracellular molecular elements for the maintenance of homeostasis in epidermal keratinocytes.
journal_name
Exp Dermatoljournal_title
Experimental dermatologyauthors
Miyazaki T,Kadono N,Konishi Y,Hagiwara N,Maekubo K,Hirai Ydoi
10.1111/exd.12278subject
Has Abstractpub_date
2013-12-01 00:00:00pages
845-7issue
12eissn
0906-6705issn
1600-0625journal_volume
22pub_type
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