Inhibitory effects of low decibel infrasound on the cardiac fibroblasts and the involved mechanism.
Inhibitory effects of low decibel infrasound on the cardiac fibroblasts and the involved mechanism.
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低分贝次声对心肌成纤维细胞的抑制作用及其机制
DOI：
10.4103/nah.nah_14_16
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发表时间：
2017-05
期刊：
影响因子：
0.7
通讯作者：
Pei ZH
中科院分区：
文献类型：
--
作者：
Jin W;Deng QQ;Chen BY;Lu ZX;Li Q;Zhao HK;Chang P;Yu J;Pei ZH
材料与方法：从Sprague-Dawley大鼠中分离培养心脏成纤维细胞。将培养的细胞分为以下四组：对照组、血管紧张素II(Ang II)组、次声组和Ang II+次声组。分别通过[3H]-胸苷和[3H]-脯氨酸掺入来评估细胞增殖和胶原合成率。通过酶联免疫吸附测定法测定TGF-β的水平。此外，采用RNAi方法分析miR-29a的生物学功能，并通过western blotting分析检测Smad3的磷酸化状态。结果：结果显示，低分贝次声显着减轻Ang II诱导的细胞增殖和胶原合成的增强。讨论：与对照相比，Ang II显着降低miR-29a的表达水平，增加TGF-β的分泌和Smad3的磷酸化，从而使Ang II的细胞增殖和胶原合成增强。通过低分贝次声波治疗部分逆转了这一情况。重要的是，miR-29a 的敲除减弱了次声对心脏成纤维细胞的影响。总之，低分贝次声通过靶向 TGF-β/Smad3 信号传导的 miR-29a 抑制 Ang II 刺激的心脏成纤维细胞。
Materials and Methods:The cardiac fibroblasts were isolated and cultured from Sprague–Dawley rats. The cultured cells were assigned into the following four groups: control group, angiotensin II (Ang II) group, infrasound group, and Ang II+ infrasound group. The cell proliferation and collagen synthesis rates were evaluated by means of [3 H]-thymidine and [3 H]-proline incorporation, respectively. The levels of TGF-β were determined by enzyme-linked immunosorbent assay. Moreover, RNAi approaches were used for the analysis of the biological functions of miR-29a, and the phosphorylation status of Smad3 was detected using western blotting analysis.Results:The results showed that low decibel infrasound significantly alleviated Ang II-induced enhancement of cell proliferation and collagen synthesis.Discussion:Compared with the control, Ang II markedly decreased the expression of miR-29a levels and increased the secretion of TGF-β and phosphorylation of Smad3, which was partly reversed by the treatment with low decibel infrasound. Importantly, knockdown of miR-29a diminished the effects of infrasound on the cardiac fibroblasts. In conclusion, low decibel infrasound inhibits Ang II-stimulated cardiac fibroblasts via miR-29a targeting TGF-β/Smad3 signaling.