|
简述线粒体电压依赖阴离子通道对携带线粒体DNA A4263G突变的细胞株线粒体钙循环的影响 |
| |
s detected by confocal images. Results Confocal imagines showed the average Rhod2 fluorescence and ΔΨm of individuals carrying tRNAIle A4263G mutation was lower than that of control group; the baseline of Rhod2 fluorescence of the control group increased after exposure to atractyloside (opener of ANT, 5 μM), but no significant change was tested on cell line from A4263G mutation. The ΔΨm decreased subsequently for both cell lines after exposure to atractyloside, while this effect of atractyloside was inhibited by VDAC blocker CsA (2 μM). Conclusions The abnormality of mitochondrial VDAC leads to increase of mitochondrial permeability and decrease of potential cell lines carrying mtDNA A4263G mutations.
【Key words】 mitochondrial DNA; voltagedependent anion channel; mitochondrial calcium cycle
Ca2+是重要的细胞信号分子，在细胞凋亡、神经、内分泌信号传导、胰岛素分泌中发挥重要作用[1]。线粒体通过2条途径影响细胞内钙代谢：①利用线粒体合成的ATP，通过钙依赖的ATP酶将钙泵出细胞，或泵入细胞内钙储存器——肌浆网(SR)、内质网(ER)。②直接通过线粒体膜上的通道蛋白摄取Ca2+。胞内钙浓度决定了线粒体对钙摄取多少，进而影响基质钙依赖脱氢酶活性和线粒体ATP合成。另外，线粒体对钙的摄取可以缓冲胞内Ca2+浓度，调节钙信号传导，还可以做为胞内钙缓冲池，避免细胞内钙超载。在细胞凋亡过程中线粒体跨膜电位的耗散主要是由于线粒体内膜的通透性转变，这是由于多个蛋白质组成的位于线粒体内膜与外膜接触位点的通透性转变孔道(PT孔道)通透性发生改变导致 [2]。PT孔道由6个部分组成：①己糖激酶;②外周苯并二(benzodiazepine)受体;③电压依赖阴离子通道(voltagedependent anion channel，VDAC);④线粒体膜间隙蛋白：肌酸激酶;⑤线粒体内膜蛋白：腺苷转运子(adenine nucleotide translocator, ANT);⑥线粒体基质蛋白：亲环蛋白D (cyclophilin D)等[34]。
为明确VDAC在携带线粒体DNA(mitochondria上一页 [1] [2] [3] [4] [5] [6] 下一页
上一个医学论文： 下肢缺血预适应后大鼠心肌中血红素加氧酶 1与炎症的变化
下一个医学论文： 对老年恶性肿瘤患者合并医院内真菌感染调查
|
|
|
|
|
|
|
您现在的位置： 绿色健康网 >> 医学论文 >> 内科论文 >> 正文