| 周浩 杨俊杰 辛婷 胡舜英 易军 周珊珊 韩天文 张颖 陈韵岱.Exendin-4 通过JNK和ERK信号通路增强大鼠脂肪来源干细胞的增殖[J].,2014,14(30):5801-5805 |
| Exendin-4 通过JNK和ERK信号通路增强大鼠脂肪来源干细胞的增殖 |
| Exendin-4 Promotes Proliferation of Adipose-derived StemCellsVia JNK and ERK Signaling Pathway |
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| DOI： |
| 中文关键词: 脂肪干细胞 Exendin-4 增殖 JNK/ERK信号通路 |
| 英文关键词: Adipose-derived stemcells Exendin-4 Proliferation JNK/ERK signaling pathway |
| 基金项目:国家高技术研究发展计划（863 计划）（2011AA020101）；国家自然科学基金面上项目（81270186） |
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| 中文摘要: |
| 目的：探讨Exendin-4对大鼠脂肪来源干细胞的（Adipose-derived stem cells，ADSCs）增殖作用及其机制。方法：体外分离培
养SD 大鼠腹股沟处脂肪组织，流式细胞学方法鉴定分离的ADSCs，使用Exendin-4（Ex-4，0-50 nm/L）对P4 代（第四代）ADSCs 进
行干预，采用MTT检测ADSCs 的增殖情况，Western blot 检测MAPK通路中JNK 和ERK 的磷酸化水平，使用相应的阻断剂来
观测JNK和ERK 通路对ADSCs 增殖作用的影响。结果：分离培养的ADSCs高表达CD29、CD90 和CD105，低表达CD31、CD34
和CD45，符合间充质干细胞的表型。Ex-4 以浓度依赖方式促进ADSCs 体外增殖，10 nm/L为最适促增殖处理浓度。同时，Ex-4 可
以提高细胞中c-Jun 和ERK的磷酸化水平，而给予相应阻断剂后，磷酸化蛋白表达减弱，细胞增殖能力也明显减弱。结论：Ex-4
可以通过JNK和ERK通路增强大鼠脂肪来源干细胞的增殖。 |
| 英文摘要: |
| Objective:To explore the effects and mechanismof Exendin-4（Ex-4）on the proliferation of adipose-derived stemcells (ADSCs).Methods:ADSCs used in this study were obtained from inguinal region in Sprague-Dawley rats and flow cytometry analysis
was conducted to detect surface antigens of ADSCs. After cells were treated with Ex-4 with different concentrations (0-50 nm/L), the
proliferation was measured with MTT test and the level of phospho-JNK and phospho-ERK were evaluated by Western blot. Next,
inhibitor of JNK and ERK signaling pathways was applied to further establish the role of JNK and ERK in Ex-4-mediated cells
proliferation.Results:ADSCs were positive for CD29, CD90 and CD105, but negative for CD31, CD34, and CD45, which was in line
with the characteristics of mescenchymal stemcells. Ex-4 could increase the proliferation of ADSCs in vitro in a concentration dependent
manner and 10 nm/L was the optimum concentration (P<0.05). Meanwhile, Ex-4 elevated the phosphorylation level of JNK and ERK.
However, application of inhibitors of JNK and ERK signaling pathway not only reversed such effects of Ex-4 on JNK and ERK, but
diminished the Ex-4-involved up-regulation of proliferation in ADSCs.Conclusion:Ex-4 increased proliferative capacity of ADSCs via
JNK and ERK signaling pathway. |
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