Cap1p attenuates the apoptosis of Candida albicans

被引：17

作者：

Dai, Bao-Di ^{[1
]}

Wang, Yan ^{[1
]}

Zhao, Lan-Xue ^{[1
]}

Li, De-Dong ^{[1
]}

Li, Ming-Bang ^{[1
]}

Cao, Yong-Bing ^{[1
]}

Jiang, Yuan-Ying ^{[1
]}

机构：

[1] Second Mil Med Univ, New Drug Res & Dev Ctr, Sch Pharm, Shanghai 200433, Peoples R China

来源：

FEBS JOURNAL | 2013年 / 280卷 / 11期

基金：

中国国家自然科学基金;

关键词：

apoptosis; Candidaalbicans; Cap1p; GLR1; reactive oxygen species; PROGRAMMED CELL-DEATH; OXIDATIVE STRESS-RESPONSE; TRANSCRIPTION FACTOR; MULTIDRUG-RESISTANCE; CYTOCHROME-C; ACETIC-ACID; GLUTATHIONE; SACCHAROMYCES; MITOCHONDRIA; AP-1;

D O I：

10.1111/febs.12251

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：

Candidaalbicans is the most common opportunistic fungal pathogen and its apoptosis is inducible by environmental stress. Based on our previous finding that transcription factor Cap1p was involved in baicalein-induced apoptosis, the present study aimed to further clarify the role of Cap1p in apoptosis by observing the impact of CAP1 deletion on cell fate. It was found that apoptotic stimulation with amphotericin B, acetic acid and hydrogen peroxide increased the number of apoptotic and necrotic cells, caspase activity and the accumulation of reactive oxygen species, whereas it decreased the mitochondrial membrane potential and intracellular ATP level in the cap1/ mutant. The cell fate was, at least partly, caused by glutathione depletion and attenuation of the expression of the glutathione reductase gene in the cap1/ mutant. Collectively, our data suggest that Cap1p participated in the apoptosis of C.albicans by regulating the expression of the glutathione reductase gene and glutathione content.

引用

页码：2633 / 2643

页数：11

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