Transient protection by peripheral benzodiazepine receptors during the early events of ultraviolet light-induced apoptosis

被引:49
作者
Stoebner, PE
Carayon, P
Casellas, P
Portier, M
Lavabre-Bertrand, T
Cuq, P
Cano, JP
Meynadier, J
Meunier, L
机构
[1] Lab Drug Toxicol, Montpellier, France
[2] CHU Nimes, Dept Cytol & Cytogenet, Nimes, France
[3] Sanofi Synthelabo Rech, Immunooncol Dept, Montpellier, France
[4] CHU Montpellier, Hop St Eloi, Dept Dermatol Allergol Photobiol, Montpellier, France
关键词
apoptosis; mitochondria; peripheral benzodiazepine receptor; ultraviolet;
D O I
10.1038/sj.cdd.4400861
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The peripheral benzodiazepine receptor (PBR) is a mitochondrial protein involved in the formation of mitochondrial permeability transition (PT) pores which play a critical role during the early events of apoptosis. PBRs are located in many tissues and are strongly expressed in the superficial layers of human epidermis. PBRs play a protective role against free radical damage and PER ligands modulate apoptosis, To investigate the role of PER during the early events of ultraviolet (UV)-mediated apoptosis we compared the effects of UVB on PBR-transfected Jurkat cells and their wild type counterparts devoid of any PER expression. Results indicate that early after UVB exposure (up to 4 h), PBR-transfected cells were more resistant to apoptosis and exhibited a delayed mitochondrial transmembrane potential drop, a diminished superoxide anions production, and a reduced caspase-3 activation. Taken together these findings suggest that PER may regulate early death signals leading to UV induced apoptosis.
引用
收藏
页码:747 / 753
页数:7
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