Sahoo Susmita, Rao K Krishnamurthy, Suraishkumar G K
Department of Chemical Engineering, Indian Institute of Technology Bombay, Powai, Mumbai, India.
Biotechnol Bioeng. 2006 May 5;94(1):118-27. doi: 10.1002/bit.20835.
Exposure of Bacillus subtilis to a shear rate of 1,482/s leads to a rapid loss of cell viability after 10 h of growth. Biochemical and molecular evidences provided below strongly suggest that cell death under high shear results from an apoptosis-like process similar to that described in eukaryotes, with activation of a caspase-3-like protease (C(3)LP) followed by DNA fragmentation. Shear stress leads to an increase in specific intracellular reactive oxygen species (siROS), possibly through activation of NADH oxidase (NOX). The formation of siROS precedes the activation of C(3)LP and DNA fragmentation, thus establishing siROS as the molecular link between shear stress and apoptosis-like cell death. A model is proposed in which NOX is viewed as being strategically placed on the plasma membrane of B. subtilis that senses and converts a mechanical force arising from shear stress into a chemical signal leading to activation of C(3)LP, DNA fragmentation, and thus, apoptosis-like cell death.
将枯草芽孢杆菌暴露于1482/秒的剪切速率下,在生长10小时后会导致细胞活力迅速丧失。以下提供的生化和分子证据有力地表明,高剪切条件下的细胞死亡源于一种类似于真核生物中所描述的凋亡样过程,即激活一种类半胱天冬酶-3蛋白酶(C(3)LP),随后发生DNA片段化。剪切应力可能通过激活NADH氧化酶(NOX)导致细胞内特定活性氧(siROS)增加。siROS的形成先于C(3)LP的激活和DNA片段化,从而确立了siROS作为剪切应力与凋亡样细胞死亡之间的分子联系。提出了一个模型,其中NOX被认为战略性地位于枯草芽孢杆菌的质膜上,它感知并将剪切应力产生的机械力转化为化学信号,导致C(3)LP激活、DNA片段化,进而引起凋亡样细胞死亡。