"Medical and Pharmaceutical Bionanotechnologies" Laboratory, Institute of Cellular Biology and Pathology "Nicolae Simionescu" of the Romanian Academy, 050568 Bucharest, Romania.
"Pathophysiology and Pharmacology" Department, Institute of Cellular Biology and Pathology "Nicolae Simionescu" of the Romanian Academy, 050568 Bucharest, Romania.
Int J Mol Sci. 2022 Mar 30;23(7):3824. doi: 10.3390/ijms23073824.
Calcific aortic valve disease (CAVD) is a progressive inflammatory disorder characterized by extracellular matrix remodeling and valvular interstitial cells (VIC) osteodifferentiation leading to valve leaflets calcification and impairment movement. Runx2, the master transcription factor involved in VIC osteodifferentiation, modulates the expression of other osteogenic molecules. Previously, we have demonstrated that the osteoblastic phenotypic shift of cultured VIC is impeded by Runx2 silencing using fullerene (C60)-polyethyleneimine (PEI)/short hairpin (sh)RNA-Runx2 (shRunx2) polyplexes. Since the use of polyplexes for in vivo delivery is limited by their instability in the plasma and the non-specific tissue interactions, we designed and obtained targeted, lipid-enveloped polyplexes (lipopolyplexes) suitable for (1) systemic administration and (2) targeted delivery of shRunx2 to osteoblast-differentiated VIC (oVIC). Vascular cell adhesion molecule (VCAM)-1 expressed on the surface of oVIC was used as a target, and a peptide with high affinity for VCAM-1 was coupled to the surface of lipopolyplexes encapsulating C60-PEI/shRunx2 (V-LPP/shRunx2). We report here that V-LPP/shRunx2 lipopolyplexes are cyto- and hemo-compatible and specifically taken up by oVIC. These lipopolyplexes are functional as they downregulate the Runx2 gene and protein expression, and their uptake leads to a significant decrease in the expression of osteogenic molecules (OSP, BSP, BMP-2). These results identify V-LPP/shRunx2 as a new, appropriately directed vehicle that could be instrumental in developing novel strategies for blocking the progression of CAVD using a targeted nanomedicine approach.
钙化主动脉瓣疾病 (CAVD) 是一种进行性炎症性疾病,其特征为细胞外基质重塑和瓣膜间质细胞 (VIC) 成骨分化,导致瓣叶钙化和运动障碍。Runx2 是 VIC 成骨分化涉及的主要转录因子,调节其他成骨分子的表达。先前,我们已经证明,使用富勒烯 (C60)-聚乙烯亚胺 (PEI)/短发夹 (sh)RNA-Runx2(shRunx2) 多聚物沉默 Runx2 会阻碍培养的 VIC 的成骨表型转变。由于多聚物在体内传递的使用受到其在血浆中的不稳定性和非特异性组织相互作用的限制,我们设计并获得了靶向脂质包被的多聚物 (lipopolyplexes),适合 (1) 系统给药和 (2) 将 shRunx2 靶向递送至成骨分化的 VIC(oVIC)。在 oVIC 表面表达的血管细胞粘附分子 (VCAM)-1 被用作靶标,并将与 VCAM-1 具有高亲和力的肽偶联到封装 C60-PEI/shRunx2(V-LPP/shRunx2)的 lipopolyplex 的表面。我们在此报告 V-LPP/shRunx2 lipopolyplex 具有细胞和血液相容性,并且可以特异性被 oVIC 摄取。这些 lipopolyplex 是功能性的,因为它们下调了 Runx2 基因和蛋白表达,并且它们的摄取导致成骨分子 (OSP、BSP、BMP-2) 的表达显著降低。这些结果表明,V-LPP/shRunx2 是一种新的、适当定向的载体,可用于通过靶向纳米医学方法开发阻止 CAVD 进展的新策略。