Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.
Exp Cell Res. 2024 Oct 1;442(2):114260. doi: 10.1016/j.yexcr.2024.114260. Epub 2024 Sep 18.
Vascular smooth muscle cell (VSMC) excessive proliferation and migration are considered the main pathological process in in-stent restenosis (ISR) following vascular intervention. Certain long noncoding RNAs play vital roles in this process. Therefore, this study aimed to explore novel regulators for ISR and further uncover the mechanism. Using a rat abdominal aorta stent implantation model, we observed that NONRATT000538.2 (NR538.2) served as a positive regulator for VSMC proliferation and migration. By manipulating NR538.2 expression via adenoviral overexpression or siRNA knockdown, we noted that NR538.2 promoted VSMC phenotypic switching, thereby inducing proliferation and migration. Significantly, the local delivery of siRNA of NR538.2 via adeno-associated virus vector suppressed balloon injury-induced neointima formation. Our study demonstrated for the first time that NR538.2 positively influenced VSMC proliferation during ISR.
血管平滑肌细胞（VSMC）的过度增殖和迁移被认为是血管介入后支架内再狭窄（ISR）的主要病理过程。某些长链非编码 RNA 在这个过程中起着至关重要的作用。因此，本研究旨在探索 ISR 的新调节因子，并进一步揭示其机制。通过大鼠腹主动脉支架植入模型，我们观察到 NONRATT000538.2（NR538.2）作为 VSMC 增殖和迁移的正调节剂。通过腺病毒过表达或 siRNA 敲低来操纵 NR538.2 的表达，我们注意到 NR538.2 促进了 VSMC 表型转换，从而诱导了增殖和迁移。值得注意的是，通过腺相关病毒载体局部递送 NR538.2 的 siRNA 抑制了球囊损伤诱导的新生内膜形成。我们的研究首次证明 NR538.2 对 ISR 期间 VSMC 的增殖有正向影响。
