肺纤维化和肺气肿合并患者肺纤维化和肺气肿组织基因表达谱的比较。

Masayuki Hanaoka, Michiko Ito, Yunden Droma, Atsuhito Ushiki, Yoshiaki Kitaguchi, Masanori Yasuo, Keishi Kubo
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引用次数: 23

摘要

背景:合并肺纤维化和肺气肿(CPFE)的特征是胸部计算机断层扫描显示肺上区肺气肿和肺下区弥漫性肺实质疾病伴纤维化。本研究的目的是通过比较CPFE患者肺纤维化和肺气肿病变的微阵列序列结果,探讨CPFE对基因表达的影响机制。结果:纤维化和肺气肿病变的表达谱在功能上有显著差异。与免疫系统、细胞骨架结构成分和细胞粘附相关的基因在纤维化病变中过度表达,而与细胞部分、细胞膜结构、血管生长和生物学、第二信使介导的信号传导和肺发育(所有有助于细胞、血管和肺的破坏和修复的过程)相关的基因在肺气肿病变中过度表达。结论:CPFE患者纤维化和肺气肿病变中存在基因表达差异。我们认为CPFE中共存的纤维化和肺气肿病变的发展是由这些不同的基因表达模式实现的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Comparison of gene expression profiling between lung fibrotic and emphysematous tissues sampled from patients with combined pulmonary fibrosis and emphysema.

Comparison of gene expression profiling between lung fibrotic and emphysematous tissues sampled from patients with combined pulmonary fibrosis and emphysema.

Comparison of gene expression profiling between lung fibrotic and emphysematous tissues sampled from patients with combined pulmonary fibrosis and emphysema.

Comparison of gene expression profiling between lung fibrotic and emphysematous tissues sampled from patients with combined pulmonary fibrosis and emphysema.

Unlabelled:

Background: Combined pulmonary fibrosis and emphysema (CPFE) is characterized by both emphysema of the upper zone and diffuse parenchymal lung disease with fibrosis of the lower zone of the lung on chest computed tomography. The aim of this study was to investigate the mechanism of CPFE regarding gene expressions by comparing the results of microarray sequences between fibrotic and emphysematous lesions in the lungs of CPFE patients.

Results: The expression profiles of the fibrotic and emphysematous lesions were remarkably different in terms of function. Genes related to the immune system, structural constituents of the cytoskeleton, and cellular adhesion were overexpressed in fibrotic lesions, while genes associated with the cellular fraction, cell membrane structures, vascular growth and biology, second-messenger-mediated signaling, and lung development (all processes that contribute to the destruction and repair of cells, vessels, and the lung) were overexpressed in emphysematous lesions.

Conclusions: The differences in gene expression were detected in fibrotic and emphysematous lesions in CPFE patients. We propose that the development of coexisting fibrotic and emphysematous lesions in CPFE is implemented by these different patterns of gene expressions.

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