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感染导致宿主细胞端粒酶活性激活及端粒延长。

Activation of telomerase activity and telomere elongation of host cells by infection.

作者信息

Liu Junlong, Zhao Shuaiyang, Li Zhi, Zhang Zhigang, Zhao Baocai, Guan Guiquan, Yin Hong, Luo Jianxun

机构信息

State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Veterinary Parasitology of Gansu Province, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, Gansu, China.

Qinghai Academy of Animal Sciences and Veterinary Medicine, Qinghai University, Xining, Qinghai, China.

出版信息

Front Microbiol. 2023 Feb 23;14:1128433. doi: 10.3389/fmicb.2023.1128433. eCollection 2023.

Abstract

-transformed cells share many phenotypes with cancer cells, including uncontrolled proliferation, immortalization, and dissemination. Telomeres are DNA-protein complex at the end of eukaryotic chromosomes that function to maintain genome stability and cell replicative capacity. Telomere length maintenance is primarily dependent on telomerase activity. In up to 90% of human cancer cells, telomerase is reactivated through expression of its catalytic subunit TERT. However, the effect of infection on telomere and telomerase activity in bovine cells has not yet been described. In the present study, we confirmed that telomere length and telomerase activity are upregulated after infection in three types of cell lines. This change depends on the presence of parasites. After eliminating from cells with antitheilerial drug buparvaquone, telomerase activity and the expression level of bTERT were decreased. In addition, inhibition of bHSP90 by novobiocin led to decreased AKT phosphorylation levels and telomerase activity, indicating that the bHSP90-AKT complex is a potent factor modulates telomerase activity in -infected cells.

摘要

转化细胞与癌细胞具有许多共同的表型,包括不受控制的增殖、永生化和扩散。端粒是真核染色体末端的DNA-蛋白质复合物,其功能是维持基因组稳定性和细胞复制能力。端粒长度的维持主要依赖于端粒酶活性。在高达90%的人类癌细胞中,端粒酶通过其催化亚基TERT的表达而重新激活。然而,感染对牛细胞中端粒和端粒酶活性的影响尚未见报道。在本研究中,我们证实了在三种细胞系感染后端粒长度和端粒酶活性上调。这种变化取决于寄生虫的存在。在用抗泰勒虫药物丁萘脒从细胞中清除寄生虫后,端粒酶活性和bTERT的表达水平降低。此外,新生霉素对bHSP90的抑制导致AKT磷酸化水平和端粒酶活性降低,表明bHSP90-AKT复合物是调节感染细胞中端粒酶活性的一个重要因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b14f/9997645/eb45fb19ca51/fmicb-14-1128433-g001.jpg

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