Yang Cheng, Li Li, Guo Junhua, Zhang Weiqiang, Zhu Wenbiao, Rao Xinhui, Huang Wenjie
Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Respiratory Medicine, Meizhou People's Hospital, Meizhou, Guangdong 514031, China.
Department of Respiratory Medicine, General Hospital of Guangzhou Military Command of Chinese PLA, Guangzhou, Guangdong 510010, China.
Pathol Res Pract. 2017 Apr;213(4):322-326. doi: 10.1016/j.prp.2017.01.018. Epub 2017 Jan 29.
Pim-3 belongs to the PIM kinase family and plays an important role in promoting inflammation, which is essential in the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD).
Immunohistochemistry (IHC), western blot, and RT-PCR analyses were performed to assess the expression of Pim-3 in both COPD and healthy lung tissue samples. SMA (Smooth Muscle Actin) and Cyclin D1 expression were detected by IHC. We also constructed animal models for the control, COPD, and Pim-3 inhibition groups, in order to analyze the effects of Pim-3 inhibition on COPD, and the role of Pim-3 in the p38 pathway.
Compared with normal lung tissue, Pim-3 mRNA and protein were up-regulated in COPD tissue. Expression of Cyclin D1 and SMA were also up-regulated in the COPD group. In the animal model experiment, we found that suppression of Pim-3 decreased Pim-3, Cyclin D1, and SMA expression, as well as ameliorated lung damage in COPD patients. The inhibition of Pim-3 also resulted in the suppression of the p38 pathway.
Our study suggests that up-regulation of Pim-3 successfully accelerated COPD development, and aggravated lung damage. The molecular mechanism of Pim-3 in COPD might be related to the p38 pathway, and is correlated with Cyclin D1 and SMA expression.
Pim-3属于PIM激酶家族，在促进炎症反应中起重要作用，而炎症反应在慢性阻塞性肺疾病（COPD）的发病机制中至关重要。
采用免疫组织化学（IHC）、蛋白质印迹法和逆转录聚合酶链反应（RT-PCR）分析，评估COPD患者和健康肺组织样本中Pim-3的表达。通过免疫组织化学检测平滑肌肌动蛋白（SMA）和细胞周期蛋白D1的表达。我们还构建了对照组、COPD组和Pim-3抑制组的动物模型，以分析Pim-3抑制对COPD的影响，以及Pim-3在p38信号通路中的作用。
与正常肺组织相比，COPD组织中Pim-3的mRNA和蛋白表达上调。COPD组中细胞周期蛋白D1和SMA的表达也上调。在动物模型实验中，我们发现抑制Pim-3可降低Pim-3、细胞周期蛋白D1和SMA的表达，并改善COPD患者的肺损伤。抑制Pim-3还导致p38信号通路的抑制。
我们的研究表明，Pim-3的上调成功加速了COPD的发展，并加重了肺损伤。Pim-3在COPD中的分子机制可能与p38信号通路有关，并且与细胞周期蛋白D1和SMA的表达相关。
