Weldon School of Biomedical Engineering, Purdue University, 206 S. Martin Jischke Drive, West Lafayette, IN, 47907, USA.
J Pept Sci. 2013 Oct;19(10):629-38. doi: 10.1002/psc.2541. Epub 2013 Aug 23.
Cell penetrating peptides (CPP) have been widely used to increase the cellular delivery of their associated cargo. Multiple modes of uptake have been identified; however, they cannot be predicted a priori. Elucidating these mechanisms is important for understanding peptide function as well as further optimizing cellular delivery. We have developed a class of mitogen activated protein kinase activated protein kinase 2 (MK2) inhibitor peptides, named FAK and YARA that utilize CPP domains to gain cellular access. In this study, we investigate the mechanism of endocytosis of these MK2 inhibitors by examining the uptake of fluorescently labeled peptide in human monocyte (THP-1) and mesothelial cells, and looking for colocalization with known markers of endocytosis. Our results indicate that uptake of the MK2 inhibitors was minimally enhanced by the addition of the fluorescent label, and that the type of endocytosis used by the inhibitor depends on several factors including concentration, cell type, and which CPP was used. We found that in THP-1 cells, the uptake of YARA occurred primarily via macropinocytosis, whereas FAK entered via all three mechanisms of endocytosis examined in this study. In mesothelial cells, uptake of YARA occurred via caveolae-mediated endocytosis, but became less specific at higher concentrations; whereas uptake of FAK occurred through clathrin-mediated endocytosis. In all cases, the delivery resulted in active inhibition of MK2. In summary, the results support endocytic uptake of fluorescently labeled FAK and YARA in two different cell lines, with the mechanism of uptake dependent on extracellular concentration, cell type, and choice of CPP.
细胞穿透肽 (CPP) 已被广泛用于提高与其相关货物的细胞递送效率。已经确定了多种摄取方式;然而,这些方式不能预先预测。阐明这些机制对于理解肽的功能以及进一步优化细胞递送都很重要。我们开发了一类丝裂原激活的蛋白激酶激活的蛋白激酶 2 (MK2) 抑制剂肽,命名为 FAK 和 YARA,它们利用 CPP 结构域进入细胞。在这项研究中,我们通过检查荧光标记肽在人单核细胞 (THP-1) 和间皮细胞中的摄取,并寻找与已知内吞作用标记物的共定位,来研究这些 MK2 抑制剂的内吞作用机制。我们的结果表明,荧光标记的添加对 MK2 抑制剂的摄取仅有微小的促进作用,并且抑制剂所采用的内吞作用类型取决于多个因素,包括浓度、细胞类型和所使用的 CPP。我们发现,在 THP-1 细胞中,YARA 的摄取主要通过巨胞饮作用发生,而 FAK 则通过本研究中检查的三种内吞作用机制进入细胞。在间皮细胞中,YARA 的摄取通过小窝蛋白介导的内吞作用发生,但在较高浓度下变得不那么特异;而 FAK 的摄取则通过网格蛋白介导的内吞作用发生。在所有情况下,递送都导致 MK2 的活性抑制。总之,这些结果支持荧光标记的 FAK 和 YARA 在两种不同细胞系中的内吞摄取,摄取机制取决于细胞外浓度、细胞类型和 CPP 的选择。