Study of the relationship between PI3K、α - SMA protein expression and idiopathic pulmonary fibrosis
Wanling Zhu, Xitao Ma, Siqin Wang
Abstract
Wanling Zhu, Xitao Ma, Siqin Wang
Abstract
Objective To study the relationship between PI3K、α - SMA protein expression and idiopathic pulmonary fibrosis. Methods 19 lung tissues were collected by open lung biopsies from patients with IPF;the control lung specimens were obtained from 18 patients undergoing thoracotomy for lung disease. Patients in the control group had no other underlying lung pathology and 5 centimeters away from the diseased region. Results The levels of the expression of PI3K、a -SMA protein were significantly higher in the IPF patients than in the control group (respectively U = 25. 000, P < 0. 01 ; U = 9.000, P < 0.01). There was positive correlation of the expression of α - SMA and PI3K protein (r =0. 823, P <0.01). Conclusion The acquisition of an apoptosis - resistant phenotype of myofibroblasts through activation of PI3K - AKT, which participate in the lung injury/repair process, may contribute to persistent or progressive lung fibrosis. Key words: Idiopathic pulmonary fibrosis; Phosphatidylinositol - 3 - kinase ; α - Smooth muscle actin; Immunohistochemistry
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Objective To study the relationship between PI3K、α - SMA protein expression and idiopathic pulmonary fibrosis. Methods 19 lung tissues were collected by open lung biopsies from patients with IPF;the control lung specimens were obtained from 18 patients undergoing thoracotomy for lung disease. Patients in the control group had no other underlying lung pathology and 5 centimeters away from the diseased region. Results The levels of the expression of PI3K、a -SMA protein were significantly higher in the IPF patients than in the control group (respectively U = 25. 000, P < 0. 01 ; U = 9.000, P < 0.01). There was positive correlation of the expression of α - SMA and PI3K protein (r =0. 823, P <0.01). Conclusion The acquisition of an apoptosis - resistant phenotype of myofibroblasts through activation of PI3K - AKT, which participate in the lung injury/repair process, may contribute to persistent or progressive lung fibrosis. Key words: Idiopathic pulmonary fibrosis; Phosphatidylinositol - 3 - kinase ; α - Smooth muscle actin; Immunohistochemistry
Key concepts: PI3K/AKT/mTOR pathway, Idiopathic pulmonary fibrosis, Medicine, Lung, SMA*, Immunohistochemistry, Myofibroblast, Pathology