Abstract | BACKGROUND: 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.
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Authors | Cheng Yang, Li Li, Junhua Guo, Weiqiang Zhang, Wenbiao Zhu, Xinhui Rao, Wenjie Huang |
Journal | Pathology, research and practice
(Pathol Res Pract)
Vol. 213
Issue 4
Pg. 322-326
(Apr 2017)
ISSN: 1618-0631 [Electronic] Germany |
PMID | 28214201
(Publication Type: Journal Article)
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Copyright | Copyright © 2017 Elsevier GmbH. All rights reserved. |
Chemical References |
- Proto-Oncogene Proteins
- PIM3 protein, human
- Pim3 protein, rat
- Protein Serine-Threonine Kinases
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Topics |
- Animals
- Blotting, Western
- Disease Models, Animal
- Humans
- Immunohistochemistry
- Male
- Protein Serine-Threonine Kinases
(metabolism)
- Proto-Oncogene Proteins
(metabolism)
- Pulmonary Disease, Chronic Obstructive
(metabolism, pathology)
- Rats
- Rats, Sprague-Dawley
- Real-Time Polymerase Chain Reaction
- Up-Regulation
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