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Molybdenum Disulfide Quantum Dots Attenuates Endothelial-to-Mesenchymal Transition by Activating TFEB-Mediated Lysosomal Biogenesis
ACS Biomaterials Science & Engineering ( IF 5.4 ) Pub Date : 2018-11-28 00:00:00 , DOI: 10.1021/acsbiomaterials.8b01253 Sunkui Ke 1 , Youlin Lai 2 , Lihuang Li 3 , Li Tu 3 , Yange Wang 3 , Lei Ren 3 , Shefang Ye 3 , Peiyan Yang 4
ACS Biomaterials Science & Engineering ( IF 5.4 ) Pub Date : 2018-11-28 00:00:00 , DOI: 10.1021/acsbiomaterials.8b01253 Sunkui Ke 1 , Youlin Lai 2 , Lihuang Li 3 , Li Tu 3 , Yange Wang 3 , Lei Ren 3 , Shefang Ye 3 , Peiyan Yang 4
Affiliation
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A defective lysosome-autophagy degradation pathway contributes to a variety of endothelial-to-mesenchymal transition (EndMT)-related cardiovascular diseases. Molybdenum disulfide quantum dots (MoS2 QDs) are nanoscale sizes in the planar dimensions and atomic structures of transition metal dichalcogenides (TMDs) materials with excellent physicochemical and biological properties, making them ideal for various biomedical applications. In this study, water-soluble MoS2 QDs with an average diameter of about 3.4 nm were synthesized by using a sulfuric acid-assisted ultrasonic method. The as-prepared MoS2 QDs exhibited low cytotoxicity of less than 100 μg/mL in both human umbilical vein endothelial cells and human coronary artery endothelial cells and showed novel biological properties to prevent EndMT and promote angiogenesis in vitro. We found that MoS2 QDs treatment-induced transcription factor (TFEB) mediated lysosomal biogenesis, which could cause autophagy activation. Importantly, using in vitro transforming growth factor (TGF)-β-induced EndMT model, we demonstrated that the cardiovascular protective effect of MoS2 QDs against EndMT acted through triggering TFEB nucleus translocation and restoring an impairment of autophagic flux, whereas genetic suppression of TFEB impaired the protective action of MoS2 QDs against EndMT. Taken together, these results gain novel insights into the mechanisms by which MoS2 QDs regulate EndMT and facilitate the development of MoS2-based nanoagents for the treatment of EndMT-related cardiovascular diseases.
中文翻译：
二硫化钼量子点通过激活TFEB介导的溶酶体生物发生来减弱内皮细胞向间充质的过渡。
缺陷的溶酶体自噬降解途径导致多种内皮向间充质转化（EndMT）相关的心血管疾病。二硫化钼量子点（MoS 2 QDs）在过渡金属二硫化碳（TMDs）材料的平面尺寸和原子结构中具有纳米级尺寸，具有出色的理化和生物学特性，使其成为各种生物医学应用的理想选择。在这项研究中，使用硫酸辅助超声方法合成了平均直径约为3.4 nm的水溶性MoS 2 QD。准备好的MoS 2QD在人脐静脉内皮细胞和人冠状动脉内皮细胞中均显示出低于100μg/ mL的低细胞毒性，并在体外具有预防EndMT和促进血管生成的新生物学特性。我们发现MoS 2 QDs治疗诱导转录因子（TFEB）介导的溶酶体生物发生，这可能会导致自噬激活。重要的是，使用体外转化生长因子（TGF）-β诱导的EndMT模型，我们证明了MoS 2 QD对EndMT的心血管保护作用通过触发TFEB核易位并恢复自噬通量受损而发挥，而遗传抑制TFEB损害了MoS 2的保护作用针对EndMT的QD。综上所述，这些结果获得了关于MoS 2 QD调节EndMT并促进基于MoS 2的纳米药物开发与EndMT相关的心血管疾病的机制的新颖见解。
更新日期：2018-11-28
中文翻译：
二硫化钼量子点通过激活TFEB介导的溶酶体生物发生来减弱内皮细胞向间充质的过渡。
缺陷的溶酶体自噬降解途径导致多种内皮向间充质转化（EndMT）相关的心血管疾病。二硫化钼量子点（MoS 2 QDs）在过渡金属二硫化碳（TMDs）材料的平面尺寸和原子结构中具有纳米级尺寸，具有出色的理化和生物学特性，使其成为各种生物医学应用的理想选择。在这项研究中，使用硫酸辅助超声方法合成了平均直径约为3.4 nm的水溶性MoS 2 QD。准备好的MoS 2QD在人脐静脉内皮细胞和人冠状动脉内皮细胞中均显示出低于100μg/ mL的低细胞毒性，并在体外具有预防EndMT和促进血管生成的新生物学特性。我们发现MoS 2 QDs治疗诱导转录因子（TFEB）介导的溶酶体生物发生，这可能会导致自噬激活。重要的是，使用体外转化生长因子（TGF）-β诱导的EndMT模型，我们证明了MoS 2 QD对EndMT的心血管保护作用通过触发TFEB核易位并恢复自噬通量受损而发挥，而遗传抑制TFEB损害了MoS 2的保护作用针对EndMT的QD。综上所述，这些结果获得了关于MoS 2 QD调节EndMT并促进基于MoS 2的纳米药物开发与EndMT相关的心血管疾病的机制的新颖见解。
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