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Mechanisms underlying dimethyl sulfoxide-induced cellular migration in human normal hepatic cells.
Environmental Toxicology and Pharmacology ( IF 4.3 ) Pub Date : 2020-09-07 , DOI: 10.1016/j.etap.2020.103489
Fengmei Wei 1 , Long Zhao 2 , Yuhong Jing 3
Affiliation  

Numerous studies have reported that low-dose dimethyl sulfoxide (DMSO, <1.5%, v/v) can interfere with various cellular processes, such as cell proliferation, differentiation, apoptosis, and cycle. By contrast, minimal information is available about the effect of low-dose DMSO on cell migration. Here, we report the effect of DMSO (0.0005%−0.5%, v/v) on cellular migration in human normal hepatic L02 cells. We used the Cell Counting Kit-8 assay to measure cell viability, scratch wound healing assay to observe cellular migration, flow cytometry to analyze cell cycle and death pattern, reverse transcription quantitative polymerase chain reaction to evaluate mRNA expression, and Western blot to detect protein levels. After treatment with 0.0005% (v/v) DMSO, more cells entered S phase arrest, the MMP1/TIMP1 ratio increased, and HSP27 expression was elevated. After treatment with 0.1% (v/v) DMSO, more cells entered G0/G1 phase arrest, the MMP2/TIMP2 ratio increased, the p-p38 and p-Smad3 signaling pathways were activated, and neuropilin-1 expression was elevated. These results showed that cells migrate when their MMP1/TIMP1 and MMP2/TIMP2 ratios are imbalanced. Such migration is modulated by the p38/HSP27 signaling pathway and TGF-β/Smad3 dependent signaling pathway.



中文翻译:

人类正常肝细胞中二甲基亚砜诱导的细胞迁移的潜在机制。

大量研究表明,低剂量的二甲基亚砜(DMSO,<1.5%,v / v)会干扰各种细胞过程,例如细胞增殖,分化,凋亡和周期。相比之下,关于低剂量DMSO对细胞迁移的影响的信息很少。在这里,我们报道了DMSO(0.0005%−0.5%,v / v)对人正常肝L02细胞中细胞迁移的影响。我们使用Cell Counting Kit-8分析法来测量细胞活力,使用刮擦伤口愈合法观察细胞迁移,使用流式细胞术分析细胞周期和死亡模式,使用逆转录定量聚合酶链反应评估mRNA表达,并使用Western blot检测蛋白质水平。用0.0005%(v / v)DMSO处理后,更多细胞进入S期停滞,MMP1 / TIMP1比增加,并且HSP27表达升高。用0.1%(v / v)DMSO处理后,更多细胞进入G0 / G1期停滞,MMP2 / TIMP2比增加,p-p38和p-Smad3信号通路被激活,神经纤毛蛋白1表达增加。这些结果表明,当细胞的MMP1 / TIMP1和MMP2 / TIMP2比例不平衡时,细胞会迁移。这种迁移受p38 / HSP27信号传导途径和TGF-β/ Smad3依赖性信号传导途径调节。

更新日期:2020-09-25
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