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首页> 外文期刊>International journal of molecular medicine >VIT1/FBXO11 knockdown induces morphological alterations and apoptosis in B10BR mouse melanocytes.
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VIT1/FBXO11 knockdown induces morphological alterations and apoptosis in B10BR mouse melanocytes.

机译：VIT1 / FBXO11敲低诱导B10BR小鼠黑素细胞形态变化和凋亡。

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It has been shown that the VIT1 gene is down-regulated in vitiligo melanocytes, but the expression of the VIT1 gene in melanocytes of Chinese patients with vitiligo and the potential function of VIT1 in pathogenesis of vitiligo are not as well known. In this study, we first compared VIT1 gene expression in melanocytes cultured from non-lesional skin of generalized vitiligo patients, normal melanocytes and melanomas in China. The cloned VIT1 ORF cDNA fragments were sequenced and then compared. VIT1 siRNAs were transfected into mouse B10BR melanocytes. The results from semi-quantitative RT-PCR demonstrated that the expression levels of VIT1 in non-lesional melanocytes from vitiligo patients are significantly lower than those in normal melanocytes. In contrast, the expression levels of VIT1 in melanoma are higher. The results also demonstrated that VIT1 is not a novel gene including a fragment of 81 bp flanking by consensus GT and AG sequences on the 5' and 3' ends, which is regarded as an intron. VIT1 without the extra intron is a known gene called FBXO11. Our findings revealed abnormal morphology by light and electron microscopes in FBXO11 siRNA transfected melancytes, which display large epithelioid perikaryon and stubby dendrites with occasional multidendricity as opposed to slender perikaryon and bipolar dendrites of controls. The electron microscopic observation indicated swelling mitochondria and endoplasmic reticulum (ER), and increased lysosomes and bubbles. Further, transfection of FBXO11 siRNA significantly promoted cell apoptosis. Collectively, this study provides comprehensive morphological proof of the relationship between dilation of ER and decreased levels of the FBXO11 gene in vitiligo melanocytes.
机译：已经表明，VIT1基因在白癜风黑素细胞中被下调，但是尚不了解中国白癜风患者黑素细胞中VIT1基因的表达以及VIT1在白癜风发病中的潜在功能。在这项研究中，我们首先比较了中国白癜风患者非病变皮肤培养的黑色素细胞，正常黑色素细胞和黑色素瘤中VIT1基因的表达。对克隆的VIT1 ORF cDNA片段进行测序，然后进行比较。将VIT1 siRNA转染到小鼠B10BR黑色素细胞中。半定量RT-PCR的结果表明，白癜风患者非病变黑素细胞中VIT1的表达水平明显低于正常黑素细胞。相反，黑素瘤中VIT1的表达水平较高。结果还表明，VIT1不是一个新颖的基因，在其5'和3'末端有侧翼共有GT和AG序列的81 bp片段，被视为内含子。没有额外内含子的VIT1是称为FBXO11的已知基因。我们的发现通过光和电子显微镜揭示了FBXO11 siRNA转染的猫鼬的异常形态，与对照的细长周核和双极树突相反，它们表现出大的上皮样周核和短枝状树突，偶尔具有多树突。电镜观察表明线粒体和内质网（ER）肿胀，溶酶体和气泡增加。此外，转染FBXO11 siRNA显着促进细胞凋亡。总的来说，这项研究为白癜风黑素细胞内质网扩张与FBXO11基因水平降低之间的关系提供了全面的形态学证据。

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