Cheng Yang1, Li Li2, Junhua Guo3, Weiqiang Zhang3, Wenbiao Zhu4, Xinhui Rao5, Wenjie Huang6. 1. Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Respiratory Medicine, Meizhou People's Hospital, Meizhou, Guangdong 514031, China. 2. Department of Respiratory Medicine, General Hospital of Guangzhou Military Command of Chinese PLA, Guangzhou, Guangdong 510010, China. 3. Department of Respiratory Medicine, Meizhou People's Hospital, Meizhou, Guangdong 514031, China. 4. Department of Pathology, Meizhou People's Hospital, Meizhou, Guangdong 514031, China. 5. Department of Thoracic Surgery, Meizhou People's Hospital, Meizhou, Guangdong 514031, China. 6. Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Respiratory Medicine, General Hospital of Guangzhou Military Command of Chinese PLA, Guangzhou, Guangdong 510010, China. Electronic address: huang69w@163.com.
Abstract
BACKGROUND: 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). METHODS: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: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). METHODS: 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. RESULTS: 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 COPDpatients. The inhibition of Pim-3 also resulted in the suppression of the p38 pathway. CONCLUSION: 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.