Sanchez-Antolín Gloria, Almohalla-Alvarez Carolina, Bueno Pilar, Almansa Raquel, Iglesias Verónica, Rico Lucia, Ortega Alicia, Muñoz-Conejero Eva, García-Pajares Felix, Bermejo-Martin Jesus F
Unidad de Hepatología, Unidad de Trasplante Hepático. Hospital Universitario Río Hortega, Valladolid, Spain.
Servicio de Análisis Clínicos, Hospital Clínico Universitario de Valladolid, Valladolid, Spain.
PLoS One. 2015 Aug 28;10(8):e0137128. doi: 10.1371/journal.pone.0137128. eCollection 2015.
The role of systemic immunity in the pathogenesis of cirrhosis is not fully understood. Analysis of transcriptomic profiles in blood is an easy approach to obtain a wide picture of immune response at the systemic level. We studied gene expression profiles in blood from thirty cirrhotic patients and compared them against those of eight healthy volunteers. Most of our patients were male [n = 21, 70%] in their middle ages [57.4 ± 6.8 yr]. Alcohol abuse was the most frequent cause of cirrhosis (n = 22, 73%). Eleven patients had hepatocellular carcinoma (36.7%). Eight patients suffered from hepatitis C virus infection (26.7%). We found a signature constituted by 3402 genes which were differentially expressed in patients compared to controls (2802 over-expressed and 600 under-expressed). Evaluation of this signature evidenced the existence of an active pro-fibrotic transcriptomic program in the cirrhotic patients, involving the [extra-cellular matrix (ECM)-receptor interaction] & [TGF-beta signaling] pathways along with the [Cell adhesion molecules] pathway. This program coexists with alterations in pathways participating in [Glycine, serine and threonine metabolism], [Phenylalanine metabolism], [Tyrosine metabolism], [ABC transporters], [Purine metabolism], [Arachidonic acid metabolism]. In consequence, our results evidence the co-existence in blood of a genomic program mediating pro-fibrotic mechanisms and metabolic alterations in advanced cirrhosis. Monitoring expression levels of the genes involved in these programs could be of interest for predicting / monitoring cirrhosis evolution. These genes could constitute therapeutic targets in this disease.
全身免疫在肝硬化发病机制中的作用尚未完全明确。分析血液中的转录组图谱是一种在全身水平获取免疫反应全貌的简便方法。我们研究了30例肝硬化患者血液中的基因表达谱,并将其与8名健康志愿者的基因表达谱进行比较。我们的大多数患者为中年男性[n = 21,70%],年龄为[57.4 ± 6.8岁]。酒精滥用是肝硬化最常见的病因(n = 22,73%)。11例患者患有肝细胞癌(36.7%)。8例患者感染丙型肝炎病毒(26.7%)。我们发现一个由3402个基因组成的特征图谱,这些基因在患者与对照组中差异表达(2802个基因过度表达,600个基因表达不足)。对该特征图谱的评估表明,肝硬化患者存在活跃的促纤维化转录组程序,涉及[细胞外基质(ECM)-受体相互作用]和[转化生长因子-β信号传导]途径以及[细胞粘附分子]途径。该程序与参与[甘氨酸、丝氨酸和苏氨酸代谢]、[苯丙氨酸代谢]、[酪氨酸代谢]、[ABC转运蛋白]、[嘌呤代谢]、[花生四烯酸代谢]途径的改变共存。因此,我们的结果证明,在晚期肝硬化患者血液中,介导促纤维化机制和代谢改变的基因组程序共存。监测这些程序中相关基因的表达水平可能有助于预测/监测肝硬化的进展。这些基因可能成为该疾病的治疗靶点。