Wang Xiaoyu, You Bin, Chen Shuo, Zhang Wenqian, Tian Bo, Li Hui
Department of Thoracic Surgery, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China.
J Thorac Dis. 2018 Mar;10(3):1765-1774. doi: 10.21037/jtd.2018.03.10.
Primary spontaneous pneumothorax (PSP) is a common disease which is often caused by the rupture of bullae in the lungs. The underlying pathogenesis of PSP remains unclear. Some molecules may be involved in the development of PSP potentially. The aim of this study was to investigate the expression of TGF-beta receptor 1 (TβR1), Smad2, Smad3 and Smad4 in the resected bullae of patients with PSP.
From May 2015 to May 2016, 34 patients with PSP underwent video-assisted thoracoscopic surgery (VATS) bullectomy. Immunohistochemistry was performed to identify the expression of TβR1, Smad2, Smad3 and Smad4 in the resected pulmonary bullae tissues. The levels of these cytokines were calculated by immunoreactivity scoring system (IRS). Ten patients without pneumothorax associated disease were selected as the control group.
The analysis showed that the expression levels of TβR1, Smad2 and Smad4 were significantly higher in bullae tissues of patients with PSP than that in normal lung tissues (P=0.012, 0.031, 0.000 respectively). There was no significant difference between the expression level of Smad3 in bullae tissue of PSP patients and that in normal lung tissues of the control group (P=0.140). However, the absolute quantity of Smad3 expression in PSP bullae tissues was (4.2529±1.7193), scored by the IRS, which is higher than that in the control lung tissues (3.2600±2.2132). Also, the expression of TβR1, Smad2, Smad3 and Smad4 were not showed correlation with the clinical characteristics of PSP patients, such as age, sex, body mass index (BMI), recurrence and side of pneumothorax.
TβR1, Smad2 and Smad4 highly expressed in bullae tissues of PSP patients. Our findings suggested that TβR1, Smad2 and Smad4 may be related to the development of PSP bullae.
原发性自发性气胸(PSP)是一种常见疾病,常由肺大疱破裂引起。PSP的潜在发病机制尚不清楚。一些分子可能潜在地参与了PSP的发生发展。本研究旨在探讨转化生长因子-β受体1(TβR1)、Smad2、Smad3和Smad4在PSP患者切除的肺大疱中的表达情况。
2015年5月至2016年5月,34例PSP患者接受了电视辅助胸腔镜手术(VATS)肺大疱切除术。采用免疫组织化学法检测切除的肺大疱组织中TβR1、Smad2、Smad3和Smad4的表达。通过免疫反应评分系统(IRS)计算这些细胞因子的水平。选取10例无气胸相关疾病的患者作为对照组。
分析显示,PSP患者肺大疱组织中TβR1、Smad2和Smad4的表达水平显著高于正常肺组织(分别为P = 0.012、0.031、0.000)。PSP患者肺大疱组织中Smad3的表达水平与对照组正常肺组织相比无显著差异(P = 0.140)。然而,通过IRS评分,PSP肺大疱组织中Smad3表达的绝对量为(4.2529±1.7193),高于对照肺组织(3.2600±2.2132)。此外,TβR1、Smad2、Smad3和Smad4的表达与PSP患者的临床特征,如年龄、性别、体重指数(BMI)、复发情况和气胸侧别均无相关性。
TβR1、Smad2和Smad4在PSP患者肺大疱组织中高表达。我们的研究结果提示,TβR1、Smad2和Smad4可能与PSP肺大疱的发生发展有关。