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水分丢失,细胞“硬化”并失去正常形态 色素沉积(溶酶体清除功能下降) 膜系统脂成分改变,流动性降低 物质合成运输与信号转导发生障碍,机械抗性降低 。 线粒体数目减少,体积增大,骨架蛋白参与的物质运输与信号转导活动减少 核膜内陷,核/染色质固缩化 ,总的复制转录活动受抑制,染色体端粒缩短,mtDNA突变增加。 蛋白质合成下降,变异蛋白出现,酶活性丧失。 细胞分裂增殖能力降低 * 凋亡小体内细胞器结构完整,线粒体、溶酶体无变化,始终有膜封闭,内溶物无释放,故不会引起炎症。 * 凋亡细胞体积变小,细胞质浓缩。凋亡Ⅰ期的细胞核内染色质高度盘绕,出现许多称为气穴现象的空泡结构。细胞凋亡的晚期,细胞核裂解为碎块,产生凋亡小体 * Commonly employed reagents and cell treatments, such as staurosporine, etoposide and UV-B irradiation cause mitochondrial membrane potential (mmp) to reduce before phosphotidylserine (PS) flipping. These changes in mmp can be detected by a range of fluorescent dyes, including carbocyanines, DiO, DilC, and TMRM and MitoTracker Red (CMXRos). All these dyes show a fall in fluorescence as mitochondrial membrane potential falls during apoptosis. * 清除受损细胞,维持内稳态 * * a?| Innate recognition of non-self involves phagocyte CD14,?2-integrins (which bind the opsonic complement fragment inactivated C3b, iC3b) and the CD91–calreticulin complex (which can bind the first component of complement, C1q, and mannose-binding lectin, MBL, which recognizes pathogen-like apoptotic-cell-associated molecular patterns, ACAMPs).?b?| Recognition of altered-self involves an array of scavenger receptors, including the class-A scavenger receptor (SRA),CD68,?LOX1?(oxidised low-density lipoprotein receptor 1) and CD36, which recognize oxidised sites on apoptotic cells that mimic oxidised low-density lipoprotein (oxLDL). Exposure of phosphatidylserine (PtdSer) on the surface of apoptotic cells is a key eat-me flag. It is detected by phagocyte phosphatidylserine receptor (PtdSerR), receptors for the bridging plasma-protein?2-glycoprotein I (2-GPI), the Mer kinase receptor for the bridging protein Gas6, and?v3?integrin (vitronectin receptor), which binds the bridging protein milk-fat globule epidermal growth factor 8 (MFGE8). Rearrangement of plasma-membrane lipids in both the dying cell and the phagocyte by the ATP-binding cassette transporter ABC1 can contribute to this type of recognition
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