Objective: To investigate the expression of mitogen-actived protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K) and hypoxia-inducible factor-1alpha (HIF-1alpha) in pulmonary artery of chronic obstructive pulmonary disease (COPD), and therefore to explore the possible roles of MAPK, PI3K and HIF-1alpha in the development of hypoxia-induced pulmonary hypertension (HPH).
Methods: Small pulmonary arterial remodeling was observed by morphometric analysis in surgically removed lung tissues from COPD patients and control patients treated for lung tumors. The expression of p-ERK, p-JNK, p-P38, p-PKB and HIF-1alpha in lung tissue was examined by in situ hybridization and immunohistochemistry.
Results: Morphometry analysis showed that the ratio of wall area to total area (WA%) and pulmonary artery media thickness (PAMT) were increased in COPD patients [18 +/- 3, (31 +/- 3) microm] than in the control [30 +/- 5, (40 +/- 4) microm, t = 7.58, 6.57, all P < 0.01]. The expression levels of p-ERK protein, p-PKB protein, HIF-1alpha protein and HIF-1alpha mRNA level (absorbance, A) were significantly higher in pulmonary artery walls of COPD patients (0.164 +/- 0.012, 0.113 +/- 0.009, 0.232 +/- 0.008, 0.154 +/- 0.013, respectively) as compared to those of the control (0.062 +/- 0.010, 0.031 +/- 0.011, 0.058 +/- 0.006, 0.052 +/- 0.008, respectively, t = 23.18, 21.03, 62.14, 2.44, all P < 0.01), while p-JNK and p-P38 protein levels in the control group (0.048 +/- 0.013, 0.028 +/- 0.007, respectively) and COPD patients (0.041 +/- 0.012, 0.031 +/- 0.010, respectively, all P > 0.05) were barely positive. The expression of p-ERK, p-PKB and HIF-1alpha were negatively correlated with LA% (r = -0.920 - -0.892, all P < 0.05), and positively correlated with PAMT (r = 0.895 - 0.934, all P < 0.05).
Conclusion: Differential expression of p-ERK, p-PKB and HIF-1alpha may be involved in the occurrence of HPH in COPD patients.
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