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铁诱导人主动脉血管平滑肌细胞钙化通过白细胞介素-24（IL-24），有/无肿瘤坏死因子-α（TNF-α）。

Iron-induced calcification in human aortic vascular smooth muscle cells through interleukin-24 (IL-24), with/without TNF-alpha.

机构信息

Department of Internal Medicine, Division of Kidney and Dialysis, Hyogo College of Medicine, 1-1 Mukogawa-Cho, Nishinomiya, Hyogo, Japan.

Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-Cho, Nishinomiya, Hyogo, Japan.

出版信息

Sci Rep. 2018 Jan 12;8(1):658. doi: 10.1038/s41598-017-19092-1.

DOI:10.1038/s41598-017-19092-1
PMID:29330517
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5766506/
Abstract

In CKD patients, arteriosclerotic lesions, including calcification, can occur in vascular smooth muscle cells in a process called Moenckeberg's medial arteriosclerosis. Iron overload induces several complications, including the acceleration of arteriosclerosis. However, the relationship between Moenckeberg's arteriosclerosis in vascular smooth muscle cells and iron accumulation has remained unknown. We tested the accelerated effect of iron on calcification in cultured human aortic vascular smooth muscle cells (HASMCs). After establishment of this model, we performed a microarray analysis using mRNA from early stage culture HASMCs after iron stimulation with or without TNF-alpha stimulation. The role of interleukin-24 (IL-24) was confirmed from candidate genes that might contribute to calcification. HASMCs demonstrated calcification induced by iron and TNF-alpha. Calcification of HASMCs was synergistically enhanced by stimulation with both iron and TNF-alpha. In the early phase of calcification, microarray analysis revealed up-regulation of IL-24. Stimulation of HASMCs by IL-24 instead of iron induced calcification. The anti-IL-24 antibody reversed the effect of IL-24, supporting the important role of IL-24 in HASMCs calcification. In conclusion, iron-induced calcification in vascular smooth muscle cells occurred via IL-24, IL-24 was increased during the calcification process induced by iron, and IL-24 itself caused calcification in the absence of iron.

摘要

在 CKD 患者中，包括钙化在内的动脉粥样硬化病变可发生在血管平滑肌细胞中，这一过程被称为莫恩克伯格中层动脉硬化症。铁过载可引发多种并发症，包括加速动脉硬化。然而，血管平滑肌细胞中的莫恩克伯格动脉硬化与铁积累之间的关系仍不清楚。我们检测了铁对培养的人主动脉血管平滑肌细胞（HASMC）钙化的加速作用。在建立该模型后，我们对铁刺激后早期培养的 HASMCs 的 mRNA 进行了微阵列分析，铁刺激的同时或不伴有 TNF-α刺激。从可能促进钙化的候选基因中证实了白细胞介素-24（IL-24）的作用。HASMCs 表现出由铁和 TNF-α诱导的钙化。铁和 TNF-α的联合刺激可协同增强 HASMCs 的钙化。在钙化的早期阶段，微阵列分析显示 IL-24 的表达上调。IL-24 刺激 HASMCs 而不是铁诱导钙化。抗 IL-24 抗体逆转了 IL-24 的作用，支持 IL-24 在 HASMCs 钙化中的重要作用。总之，铁诱导的血管平滑肌细胞钙化是通过 IL-24 发生的，在铁诱导的钙化过程中 IL-24 增加，而 IL-24 本身在没有铁的情况下也可引起钙化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/740dc36e47ba/41598_2017_19092_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/07cf4b86dd36/41598_2017_19092_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/9ea127e7ca6c/41598_2017_19092_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/861bc473ee29/41598_2017_19092_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/3cf90b2470b2/41598_2017_19092_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/8a535cff22e3/41598_2017_19092_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/740dc36e47ba/41598_2017_19092_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/07cf4b86dd36/41598_2017_19092_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/9ea127e7ca6c/41598_2017_19092_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/861bc473ee29/41598_2017_19092_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/3cf90b2470b2/41598_2017_19092_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/8a535cff22e3/41598_2017_19092_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a75/5766506/740dc36e47ba/41598_2017_19092_Fig6_HTML.jpg

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