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首页> 外文期刊>Life sciences >Expression profile of the sphingosine kinase signalling system in the lung of patients with chronic obstructive pulmonary disease.
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Expression profile of the sphingosine kinase signalling system in the lung of patients with chronic obstructive pulmonary disease.

机译：鞘氨醇激酶信号传导系统在慢性阻塞性肺疾病患者肺中的表达谱。

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AIMS: Chronic obstructive pulmonary disease (COPD) is a leading cause of death worldwide. Despite its importance, treatment methods are limited and restricted to symptomatic care, highlighting the urgent need for new treatment options. Tissue damage in COPD is thought to result from an inability of the normal repair processes with accumulation of apoptotic material and impaired clearance of this material by macrophages in the airways. Lung inflammation involves the bioactive sphingolipid sphingosine 1-phosphate (S1P). MAIN METHODS: We investigated lung tissue samples from 55 patients (25 with COPD) undergoing lobectomies for management of cancer. We analysed the sphingosine-kinase (SphK) mRNA expression profile, SphK enzyme activity as well as the localisation and expression of individual proteins related to the SphK-signalling system. KEY FINDINGS: We show in this study for the first time a comprehensive expression profile of all synthesising enzymes, receptors and degrading enzymes of the SphK-signalling system in the human lung. Multivariate ANOVA showed that the relative mRNA expression of S1P receptor (S1PR) subtype 5 was reduced in COPD. There were strong positive correlations between the mRNA expression of S1PR5 and S1PR1 and S1PR3, and between S1PR3 and S1PR2. A significant negative correlation was found between S1PR1 and SphK protein activity. SIGNIFICANCE: The correlations between expression levels of receptors and enzymes involved in the sphingosine kinase signalling system in the lung suggest common regulatory mechanisms. Our findings of reduced S1PR5 in COPD and the correlation with other S1P receptors in COPD identify S1PR5 as a possible novel target for pharmacotherapy.
机译：目的：慢性阻塞性肺疾病（COPD）是世界范围内主要的死亡原因。尽管很重要，但治疗方法仍然有限，并且仅限于对症治疗，这凸显了对新治疗方案的迫切需求。认为COPD中的组织损伤是由于正常的修复过程无法进行而导致的，该过程包括凋亡物质的积累以及气道中巨噬细胞对该物质的清除能力的损害。肺部炎症涉及具有生物活性的鞘脂鞘氨醇1-磷酸（S1P）。主要方法：我们调查了55名接受肺叶切除术的患者（25名COPD）的肺组织样本，以管理癌症。我们分析了鞘氨醇激酶（SphK）mRNA表达谱，SphK酶活性以及与SphK信号转导系统相关的单个蛋白质的定位和表达。主要发现：我们首次在这项研究中显示人肺中SphK信号传导系统的所有合成酶，受体和降解酶的全面表达谱。多元方差分析表明COPD中S1P受体（S1PR）5亚型的相对mRNA表达降低。 S1PR5和S1PR1和S1PR3的mRNA表达之间以及S1PR3和S1PR2的mRNA表达之间有很强的正相关。发现S1PR1和SphK蛋白活性之间显着负相关。意义：参与鞘氨醇激酶信号转导系统的受体和酶的表达水平之间的相关性提示了常见的调节机制。我们发现COPD中S1PR5减少以及与COPD中其他S1P受体的相关性发现，S1PR5是药物治疗的新靶标。

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