title: Up-regulation of Pim-3 in Chronic Obstructive Pulmonary Disease (COPD) patients and its potential therapeutic role in COPD rat modeling.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Respiratory Medicine, Meizhou People's Hospital, Meizhou, Guangdong 514031, China.
authors.forename: Cheng
authors.initials: C
authors.lastname: Yang
authors.affiliation: Department of Respiratory Medicine, General Hospital of Guangzhou Military Command of Chinese PLA, Guangzhou, Guangdong 510010, China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Respiratory Medicine, Meizhou People's Hospital, Meizhou, Guangdong 514031, China.
authors.forename: Junhua
authors.initials: J
authors.lastname: Guo
authors.affiliation: Department of Respiratory Medicine, Meizhou People's Hospital, Meizhou, Guangdong 514031, China.
authors.forename: Weiqiang
authors.initials: W
authors.lastname: Zhang
authors.affiliation: Department of Pathology, Meizhou People's Hospital, Meizhou, Guangdong 514031, China.
authors.forename: Wenbiao
authors.initials: W
authors.lastname: Zhu
authors.affiliation: Department of Thoracic Surgery, Meizhou People's Hospital, Meizhou, Guangdong 514031, China.
authors.forename: Xinhui
authors.initials: X
authors.lastname: Rao
authors.affiliation: 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.
authors.forename: Wenjie
authors.initials: W
authors.lastname: Huang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D004195:Disease Models, Animal; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D029424:Pulmonary Disease, Chronic Obstructive / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D015854:Up-Regulation
chemical_list: D011518:Proto-Oncogene Proteins; C499249:PIM3 protein, human; C113398:Pim3 protein, rat; D017346:Protein Serine-Threonine Kinases
keywords: COPD rat modeling; Chronic obstructive pulmonary disease; Pim-3; p38