Banfalvi Gaspar
Department of Biotechnology and Microbiology, University of Debrecen, 1 Egyetem Square, Debrecen, 4010, Hungary.
Apoptosis. 2017 Feb;22(2):169-174. doi: 10.1007/s10495-016-1328-0.
Dying cells subjected to apoptotic programs are engulfed by neighboring cells or by professional phagocytes, without inflammation or immunological reactions in the tissue where apoptosis takes place. Apoptotic cells release danger-associated project signals to their neighbours, through different molecular patterns, stimulate antigen production and immune responses. Microenvironmental effects with several functional consequences indicate that cell death is a complex process and may take place in several ways. This idea is expressed by the title of the Special Issue and by the title of the guest editorial "Mille modis morimur" meaning that not only multicellular organisms, but also single cells may die in a thousand ways. This idea is demonstrated by the papers serving as examples for cell death. Apoptosis was induced by clary sage oil in Candida cells. Heavy metal (Gd) induced cell motility and apoptosis was found in mammalian cells. RNA oxidation enhanced the reversion frequency of apoptosis in yeast mutants. The frequency of apoptotic micronucleus formation increased in a concentration-dependent manner by methotrexate. The antioxidant coenzyme Q10 protected renal proximal tubule cells against nicotine-induced apoptosis. The synergy of 2-deoxy-D-glucose combined with berberine induced lysosome/autophagy. The mitochondrial apoptotic pathway could be regulated by glucocorticoid receptor in collaboration with Bcl-2 family proteins in developing T cells. Cylindrospermopsin induced biochemical changes led to apoptosis in plants. Mechanisms of stress seriously impacted the risk of apoptosis. Transcriptional control of apoptotic cell clearance was achieved by macrophage nuclear receptors. Finally, the clinical aspects of apoptosis-induced lymphopenia were reviewed in sepsis and other severe injuries. These examples not only support the view of many ways of cell death, but predict further potential ways to induce or reduce the risk of cell death.
经历凋亡程序的濒死细胞会被邻近细胞或专业吞噬细胞吞噬,在发生凋亡的组织中不会引发炎症或免疫反应。凋亡细胞通过不同分子模式向其邻居释放危险相关的投射信号,刺激抗原产生和免疫反应。具有多种功能后果的微环境效应表明,细胞死亡是一个复杂的过程,可能以多种方式发生。这一观点体现在特刊的标题以及客座编辑的标题“Mille modis morimur”中,意思是不仅多细胞生物,单细胞也可能以千种方式死亡。作为细胞死亡示例的论文证明了这一观点。鼠尾草油在念珠菌细胞中诱导凋亡。重金属(钆)诱导哺乳动物细胞的细胞运动并发现凋亡现象。RNA氧化提高了酵母突变体中凋亡的回复频率。甲氨蝶呤使凋亡微核形成频率呈浓度依赖性增加。抗氧化剂辅酶Q10保护肾近端小管细胞免受尼古丁诱导的凋亡。2-脱氧-D-葡萄糖与黄连素联合的协同作用诱导溶酶体/自噬。在发育中的T细胞中,线粒体凋亡途径可由糖皮质激素受体与Bcl-2家族蛋白协同调节。柱孢藻毒素诱导的生化变化导致植物凋亡。应激机制严重影响凋亡风险。巨噬细胞核受体实现了对凋亡细胞清除的转录控制。最后,综述了脓毒症和其他严重损伤中凋亡诱导淋巴细胞减少的临床方面。这些例子不仅支持细胞死亡有多种方式的观点,还预测了诱导或降低细胞死亡风险的更多潜在方式。