以前,我们成功地 poly 准备了(vinyldiaminotriazine )(PVDT ) 基于经由与腺嘌胸腺嘧啶结合的氢的原生质标志 DNA complexed 基于对的非病毒的向量。在这份报告,表面费用和这个系统的复杂尺寸进一步被检验。结果证明那基于 PVDT 的聚合物能盖住导致稍微否定或中立的建筑群的 DNA 的表面费用。复杂尺寸被二个事件管理,这也被发现:聚集由中立粒子的不稳定性导致了,并且更紧缩的建筑群由基于 PVDT 的聚合物生产了。在细胞的举起的学习,在 III 的氯普马嗪和弹指被用来分别地禁止调停 clathrin 、调停 caveolae 的 endocytosis。我们发现基于 PVDT 的系统经由 non-clathrin 被搬运进房间, non-caveolae 调停了 endocytosis。这个特殊过程被温度抑制和动力学试金学习。如此的一条小径被(i) 描绘,这被揭示一个更多的精力依赖者过程并且(i i ) 慢 transfection 有效的成为主观。
Previously we successfully prepared poly(vinyldiaminotriazine)(PVDT)-based non-viral vectors which complexed piasmid DNA via hydrogen bonding with adenine-thymine base pairs, in this report, surface charges and complex sizes of this system were further examined. The results showed that PVDT-based polymer could cover surface charges of DNA resulting in slightly negative or neutral complexes. It was also found that the complex sizes were governed by two events: the aggregation induced by the instability of neutral particles, and more compact complexes produced by PVDT-based polymers. In the study of cellular uptake, chlorpromazine and filipin III were used to inhibit clathrin-and caveolae-mediated endocytosis, respectively. We found that PVDT-based systems were transported into cells via a non-clathrin, non-caveolae mediated endocytosis. This special process was studied by temperature inhibition and kinetics assays. It was revealed that such a pathway was characterized by (i) a more en- ergy dependent process and (ii) a much slow transfection-effective internalization.