Lee Mi-Ae, Kim Jeong-A, Shin Mee-Young, Lee Jeong K, Park Soon-Jung, Lee Kyu-Ho
Department of Life Science, Sogang University, Seoul 121-742, Republic of Korea.
J Microbiol Biotechnol. 2015 Feb;25(2):302-6. doi: 10.4014/jmb.1501.01007.
VvpM, one of the extracellular metalloproteases produced by Vibrio vulnificus, induces apoptotic cell death via a pathway consisting of ERK activation, cytochrome c release, and activation of caspases-9 and -3. VvpM-treated cells also showed necrotic cell death as stained by propidium iodide (PI). The percentage of PI-stained cells was decreased by pretreatment with Necrostatin-1, indicating that VvpM-mediated cell death occurs through necroptosis. The appearance of autophagic vesicles and lipidated form of light-chain-3B in rVvpM-treated cells suggests an involvement of autophagy in this process. Therefore, the multifarious action of VvpM might be one of the factors responsible for V. vulnificus pathogenesis.
创伤弧菌产生的细胞外金属蛋白酶之一VvpM，通过由ERK激活、细胞色素c释放以及半胱天冬酶-9和-3激活组成的途径诱导凋亡性细胞死亡。经VvpM处理的细胞经碘化丙啶（PI）染色后也显示出坏死性细胞死亡。用Necrostatin-1预处理可降低PI染色细胞的百分比，表明VvpM介导的细胞死亡是通过坏死性凋亡发生的。经重组VvpM处理的细胞中自噬小泡的出现和轻链3B的脂化形式表明自噬参与了这一过程。因此，VvpM的多种作用可能是创伤弧菌发病机制的因素之一。
