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Unravelling the Role of MAPKs (ERK1/2) in Venous Reflux in Patients with Chronic Venous Disorder
Cells Tissues Organs ( IF 2.7 ) Pub Date : 2018-01-01 , DOI: 10.1159/000500449
Miguel A Ortega 1, 2 , Ángel Asúnsolo 2, 3 , Beatriz Romero 1, 2 , María J Álvarez-Rocha 1 , Felipe Sainz 4 , Javier Leal 5 , Melchor Álvarez-Mon 1, 2, 6 , Julia Buján 7, 8 , Natalio García-Honduvilla 1, 2, 9
Affiliation  

Chronic venous disorder (CVeD), is a disorder in which there is a modification in the conditions of blood return to the heart. The disorder may arise from incompetent valves and the resultant venous reflux (chronic venous insufficiency, CVI). The economic burden of CVeD on health systems is high, and research efforts have sought to elucidate the mechanisms involved as possible therapeutic targets. The mitogen-activated protein kinase (MAPK) enzymes mediate a wide array of physiopathological processes in human tissues. In this family of proteins, extracellular signal-regulated kinase (ERK)1/2 plays a direct role in the cell homeostasis that determines the viability of mammalian tissues. This study sought to examine whether ERK1/2 plays a role in venous reflux. This was a prospective study performed on 56 participants including 11 healthy controls. Of the CVeD patients, 23 had venous reflux with CVI (CVI-R) and 22 had no reflux (NR). Distribution by age was: controls <50 years (n = 4) and ≥50 years (n = 7); NR <50 years (n = 9) and ≥50 years (n = 13); CVI-R <50 years (n = 11) and ≥50 years (n = 12). Great saphenous vein specimens were subjected to gene (real-time polymerase chain reaction, RT-qPCR) and protein (immunohistochemistry, IHC) expression techniques to identify ERK1/2. Data was compared between groups using the Mann Whitney U test. Patients with CVI showed significant gene activation of ERK1/2 protein, and, in those with venous reflux, the expression of this gene was significantly greater. The CVI-R group <50 years showed significantly greater ERK1/2 gene expression than their age-matched controls. Expression patterns were consistent with IHC findings. Our studies suggest that ERK1/2 expression is involved in venous vascular disease.

中文翻译:

阐明 MAPKs (ERK1/2) 在慢性静脉疾病患者静脉反流中的作用

慢性静脉疾病 (CVeD) 是一种血液回流心脏状况发生改变的疾病。这种疾病可能源于瓣膜功能不全和由此产生的静脉反流(慢性静脉功能不全,CVI)。CVeD 对卫生系统的经济负担很高,研究工作试图阐明作为可能的治疗目标所涉及的机制。丝裂原活化蛋白激酶 (MAPK) 酶介导了人体组织中的一系列病理生理过程。在这个蛋白质家族中,细胞外信号调节激酶 (ERK)1/2 在决定哺乳动物组织活力的细胞稳态中起直接作用。本研究试图检查 ERK1/2 是否在静脉反流中起作用。这是一项对 56 名参与者进行的前瞻性研究,其中包括 11 名健康对照。在 CVeD 患者中,23 名有 CVI 的静脉反流 (CVI-R),22 名没有反流 (NR)。年龄分布为:对照<50 岁(n = 4)和≥50 岁(n = 7);NR <50 年(n = 9)和≥50 年(n = 13);CVI-R <50 年(n = 11)和≥50 年(n = 12)。对大隐静脉标本进行基因(实时聚合酶链反应,RT-qPCR)和蛋白质(免疫组织化学,IHC)表达技术以鉴定 ERK1/2。使用 Mann Whitney U 检验比较组间数据。CVI 患者表现出显着的 ERK1/2 蛋白基因激活,并且在静脉反流患者中,该基因的表达显着增加。与年龄匹配的对照组相比,CVI-R 组 <50 岁的 ERK1/2 基因表达显着增加。表达模式与 IHC 发现一致。
更新日期:2018-01-01
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