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自噬调节蛋白酶体抑制剂诱导的人胚胎干细胞来源的视网膜色素上皮细胞色素沉着。

Autophagy Regulates Proteasome Inhibitor-Induced Pigmentation in Human Embryonic Stem Cell-Derived Retinal Pigment Epithelial Cells.

作者信息

Juuti-Uusitalo Kati, Koskela Ali, Kivinen Niko, Viiri Johanna, Hyttinen Juha M T, Reinisalo Mika, Koistinen Arto, Uusitalo Hannu, Sinha Debasish, Skottman Heli, Kaarniranta Kai

机构信息

Faculty of Medicine and Life Sciences, BioMediTech, University of Tampere, 33014 Tampere, Finland.

Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, 70211 Kuopio, Finland.

出版信息

Int J Mol Sci. 2017 May 19;18(5):1089. doi: 10.3390/ijms18051089.

Abstract

The impairment of autophagic and proteasomal cleansing together with changes in pigmentation has been documented in retinal pigment epithelial (RPE) cell degeneration. However, the function and co-operation of these mechanisms in melanosome-containing RPE cells is still unclear. We show that inhibition of proteasomal degradation with MG-132 or autophagy with bafilomycin A1 increased the accumulation of premelanosomes and autophagic structures in human embryonic stem cell (hESC)-derived RPE cells. Consequently, upregulation of the autophagy marker p62 (also known as sequestosome-1, SQSTM1) was confirmed in Western blot and perinuclear staining. Interestingly, cells treated with the adenosine monophosphatedependent protein kinase activator, AICAR (5-Aminoimidazole-4-carboxamide ribonucleotide), decreased the proteasome inhibitor-induced accumulation of premelanosomes, increased the amount of autophagosomes and eradicated the protein expression of p62 and LC3 (microtubule-associated protein 1A/1B-light chain 3). These results revealed that autophagic machinery is functional in hESC-RPE cells and may regulate cellular pigmentation with proteasomes.

摘要

自噬和蛋白酶体清除功能受损以及色素沉着变化已在视网膜色素上皮(RPE)细胞变性中得到证实。然而,这些机制在含黑素小体的RPE细胞中的功能及协同作用仍不清楚。我们发现,用MG-132抑制蛋白酶体降解或用巴弗洛霉素A1抑制自噬会增加人胚胎干细胞(hESC)来源的RPE细胞中前黑素小体和自噬结构的积累。因此,在蛋白质印迹和核周染色中证实了自噬标志物p62(也称为聚集体蛋白1,SQSTM1)的上调。有趣的是,用单磷酸腺苷依赖性蛋白激酶激活剂AICAR(5-氨基咪唑-4-甲酰胺核糖核苷酸)处理的细胞减少了蛋白酶体抑制剂诱导的前黑素小体积累,增加了自噬体数量,并消除了p62和LC3(微管相关蛋白1A/1B轻链3)的蛋白表达。这些结果表明,自噬机制在hESC-RPE细胞中起作用,并且可能与蛋白酶体一起调节细胞色素沉着。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e360/5454998/ed378f5bd28e/ijms-18-01089-g001.jpg

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