Objective:To construct CD106-targeted RNAi lentiviral vector plasmids. Methods:4 targets aimed at CD106(Target 1, 2, 3, 4)were designed. Oligo-DNA fragment containing short hairpin frame was synthesized and reannealed, and then cloned into lentivi-ral expression vector. PCR and sequencing analysis were made for verifying the positive clones. The virus packaging plasmids were trans-fected into 293T cells to harvest siRNA lentivirus. After infection in HN12 cells, Real-time PCR and western blot were performed to de-termine the expressing level of CD106. Results:PCR and sequencing revealed that siRNA plasmids was correctly constructed. Virus with a titer of 1 × 109 TU/ml was successfully packaged at least. CD106 expression in HN12 cells could be knockdown by virus infection sig-nifically, compared with negative control lentivirus. Conclusion: The recombinant lentiviral siRNA expressing vector targeting human CD106 gene has been successfully constructed and packaged. CD106 gene in cells may be down-regulated by lentiviral siRNA.

Dental pulp stem cells (DPSC) are pluripotent stem cells with high differentiation potential isolated from dental pulp. Using DPSC for vascular regeneration may be a good option. Hypoxia inducible factor-1α (HIF-1α) is an upstream gene of vascular endothelial growth factor (VEGF), and the small ubiquitin like protease 1 (SENP1) can reverse the small ubiquitin like (SUMO) modification of HIF-1α. Through the regulation of SENP1/HIF-1α, good vascular regeneration characteristics have been demonstrated in many in vitro and in vivo experiments. The SENP1/HIF-1α signaling axis has varying degrees of promoting and inhibiting effects on many solid tumors. Although there is relatively little literature on the role of the SENP1/HIF-1α signaling axis in dental pulp stem cells, it can be determined that SENP1/HIF-1α plays an important role in the angiogenesis of dental pulp stem cells. This article will elucidate the SENP1/HIF-1α signaling pathway and its mechanism of promoting vascular differentiation of DPSC.