Soldano Stefano, Paolino Sabrina, Pizzorni Carmen, Trombetta Amelia Chiara, Montagna Paola, Brizzolara Renata, Corallo Claudio, Giordano Nicola, Sulli Alberto, Cutolo Maurizio
Research Laboratory and Academic Division of Clinical Rheumatology, Department of Internal Medicine, University of Genova, IRCCS AOU San Martino Hospital, Genoa, Italy.
Department of Medicine, Surgery and Neurosciences, Scleroderma Unit, University of Siena, Italy.
Clin Exp Rheumatol. 2017 May-Jun;35(3):484-493. Epub 2017 Jan 27.
To evaluate the ability of dual endothelin (ET) receptor antagonists (ETA/ETB -ETA/BRAs) to contrast the ET-1-induced effects on cultured human microvascular endothelial cells (HMVECs).
Some cultured HMVECs were untreated, or treated with ET-1 (100nM) or transforming growth factor β1 (TGFβ1, 10ng/mL) alone for 6 days, in order to induce the endothelial-to-mesenchymal transition (EndoMT). Other cultured HMVECs were pre-treated for 1hr with ETA/BRAs bosentan (10μM) or macitentan (1μM, 10μM) before the stimulation with ET-1 for 6 days. At the end of treatments, a mechanical injury was induced to cultured HMVECs (by scratching the cell monolayer with a sterile tip), and then the cell ability to re-fill the damaged area was determined after 24hrs. EndoMT phenotype markers and monocyte chemoattractant protein-1 (MCP-1) were evaluated by qRT-PCR and Western blotting. Statistical analysis was performed using Mann-Whitney-U non-parametric test.
Both ET-1 and TGFβ1 induced EndoMT and the MCP-1 over-expression in cultured HMVECs, as well as reduced the process of endothelial cell damage repair. Pre-treatment with ETA/BRAs let cultured HMVECs to significantly restore the in vitro damage of the cell monolayer and antagonised the EndoMT process as well as the MCP-1 over-expression (range p<0.05 - p<0.001). Conversely, untreated or TGFβ1-treated HMVECs were found unaffected by the ETA/BRAs treatments.
The treatment with dual ETA/BRAs seems to partially restore the altered cell function induced by ET-1 in cultured endothelial cells, and might justify their therapeutic efficiency in clinical conditions characterised by increased concentrations of ET-1.
评估双重内皮素(ET)受体拮抗剂(ETA/ETB -ETA/BRAs)对抗ET-1对培养的人微血管内皮细胞(HMVECs)所产生影响的能力。
一些培养的HMVECs未作处理,或单独用ET-1(100nM)或转化生长因子β1(TGFβ1,10ng/mL)处理6天,以诱导内皮-间充质转化(EndoMT)。其他培养的HMVECs在用ET-1刺激6天之前,先用ETA/BRAs波生坦(10μM)或马西替坦(1μM、10μM)预处理1小时。在处理结束时,对培养的HMVECs诱导机械损伤(用无菌吸头刮擦细胞单层),然后在24小时后测定细胞重新填充受损区域的能力。通过qRT-PCR和蛋白质印迹法评估EndoMT表型标志物和单核细胞趋化蛋白-1(MCP-1)。使用曼-惠特尼-U非参数检验进行统计分析。
ET-1和TGFβ1均诱导培养的HMVECs发生EndoMT和MCP-1过表达,并降低了内皮细胞损伤修复过程。用ETA/BRAs预处理可使培养的HMVECs显著恢复细胞单层的体外损伤,并对抗EndoMT过程以及MCP-1过表达(范围p<0.05 - p<0.001)。相反,未处理或经TGFβ1处理的HMVECs不受ETA/BRAs处理的影响。
双重ETA/BRAs治疗似乎部分恢复了ET-1在培养的内皮细胞中诱导的细胞功能改变,这可能证明它们在ET-1浓度升高的临床情况下具有治疗效果。