MicroRNA-21, induced by high glucose, modulates macrophage apoptosis via programmed cell death 4.
MicroRNA-21, induced by high glucose, modulates macrophage apoptosis via programmed cell death 4.
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DOI：
10.3892/mmr.2015.3398
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发表时间：
2015-07
影响因子：
3.4
通讯作者：
Yuan-Yuan Shang-Yuan;Ning-ning Fang;Feng Wang;Hui Wang;Zhi-hao Wang;Mengxiong Tang;Jie Peng;Yun Zhang;Wei Zhang;M. Zhong
中科院分区：
文献类型：
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作者：
Yuan-Yuan Shang-Yuan;Ning-ning Fang;Feng Wang;Hui Wang;Zhi-hao Wang;Mengxiong Tang;Jie Peng;Yun Zhang;Wei Zhang;M. Zhong
MicroRNA-21 （miR-21）被发现能促进细胞增殖和存活。它也被证明在许多形式的心血管疾病中表达增加。然而，miR-21参与动脉粥样硬化的机制仍有待阐明。在本研究中，我们证明了miR-21在Raw 264.7巨噬细胞中响应高浓度葡萄糖刺激时以时间依赖的方式上调。高浓度葡萄糖诱导巨噬细胞凋亡。在正常浓度的葡萄糖处理下，miR-21抑制的巨噬细胞表现出细胞凋亡水平的增加和活化的caspase-3水平的增强，而在miR-21抑制剂和高浓度葡萄糖处理下，细胞凋亡水平显著增加。此外，miR-21的抑制增加了程序性细胞死亡4 （PDCD4）的mRNA和蛋白质水平，相比之下，在高浓度葡萄糖处理的miR-21抑制细胞中，PDCD4的mRNA和蛋白质水平降低。综上所述，miR-21在巨噬细胞中对高浓度葡萄糖处理敏感，并且似乎对高浓度葡萄糖通过PDCD4诱导的巨噬细胞凋亡具有保护作用。
MicroRNA-21 (miR-21) has been found to promote cell proliferation and survival. It has also been shown to exhibit an increased expression in a number of forms of cardiovascular disease. However, the mechanisms underlying the involvement of miR-21 in atherosclerosis remain to be elucidated. In the present study, it was demonstrated that miR-21 was upregulated in a time-dependent manner in response to high-concentration glucose stimulation in Raw 264.7 macrophages. High concentrations of glucose induce macrophage apoptosis. miR-21-inhibited macrophages treated with a normal concentration of glucose exhibited increased levels of cell apoptosis and augmented levels of activated caspase-3, while cells treated with an miR-21 inhibitor and a high concentration of glucose, revealed significantly increased levels of apoptosis. In addition, inhibition of miR-21 increased mRNA and protein levels of programmed cell death 4 (PDCD4), which, by contrast, were reduced in miR-21-inhibited cells that had been treated with a high concentration of glucose. In conclusion, miR-21 is sensitive to high-concentration glucose treatment in macrophages, and appears to have a protective effect in macrophage apoptosis induced by high concentrations of glucose via PDCD4.