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甲氨蝶呤调节EA.hy 926细胞中的叶酸表型和炎症特征。

Methotrexate modulates folate phenotype and inflammatory profile in EA.hy 926 cells.

作者信息

Summers Carolyn M, Hammons Andrea L, Arora Jasbir, Zhang Suhong, Jochems Jeanine, Blair Ian A, Whitehead Alexander S

机构信息

Centers for Cancer Pharmacology, Pharmacogenetics, and Excellence in Environmental Toxicology, Department of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.

Centers for Cancer Pharmacology, Pharmacogenetics, and Excellence in Environmental Toxicology, Department of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, United States.

出版信息

Eur J Pharmacol. 2014 Jun 5;732:60-7. doi: 10.1016/j.ejphar.2014.03.004. Epub 2014 Mar 18.

DOI:10.1016/j.ejphar.2014.03.004
PMID:24657277
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4402228/
Abstract

EA.hy 926 cells grown under low folate conditions adopt a "pro-atherosclerotic" morphology and biochemical phenotype. Pharmacologically relevant doses of the antifolate drug methotrexate (MTX) were applied to EA.hy 926 cells maintained in normal (Hi) and low (Lo) folate culture media. Under both folate conditions, MTX caused inhibition of cell proliferation without significantly compromising metabolic activity. MTX treated Hi cells were depleted of folate derivatives, which were present in altered proportions relative to untreated cells. Transcript profiling using microarrays indicated that MTX treatment modified the transciptome in similar ways for both Hi and Lo cells. Many inflammation-related genes, most prominently those encoding C3 and IL-8, were up-regulated, whereas many genes involved in cell division were down-regulated. The results for C3 and IL-8 were confirmed by quantitative RT-PCR and ELISA. MTX appears to modify the inflammatory potential of EA.hy 926 cells such that its therapeutic properties may, at least under some conditions, be accompanied by the induction of a subset of gene products that promote and/or maintain comorbid pathologies.

摘要

在低叶酸条件下培养的EA.hy 926细胞呈现出“促动脉粥样硬化”的形态和生化表型。将具有药理学相关性剂量的抗叶酸药物甲氨蝶呤（MTX）应用于在正常（高叶酸，Hi）和低叶酸（Lo）培养基中培养的EA.hy 926细胞。在两种叶酸条件下，MTX均能抑制细胞增殖，且不会显著损害代谢活性。MTX处理的Hi细胞中的叶酸衍生物被耗尽，与未处理细胞相比，其比例发生了改变。使用微阵列进行转录谱分析表明，MTX处理对Hi细胞和Lo细胞的转录组产生了相似的影响。许多与炎症相关的基因，最显著的是编码C3和IL-8的基因，被上调，而许多参与细胞分裂的基因被下调。C3和IL-8的结果通过定量RT-PCR和ELISA得到证实。MTX似乎改变了EA.hy 926细胞的炎症潜能，使得其治疗特性在至少某些情况下可能伴随着诱导促进和/或维持合并症的一组基因产物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/50d6eacef16d/nihms578031f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/d30328ac77d4/nihms578031f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/6f336c14be26/nihms578031f2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/3231593b5aa9/nihms578031f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/066232caa8bf/nihms578031f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/50d6eacef16d/nihms578031f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/d30328ac77d4/nihms578031f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/6f336c14be26/nihms578031f2a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/3231593b5aa9/nihms578031f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/066232caa8bf/nihms578031f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7681/4402228/50d6eacef16d/nihms578031f5.jpg

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