ABI3BP差异化调节中膜SMCs和血管外膜Sca-1+祖细胞功能影响内膜新生的作用及机制

血管重构是血管成形术后再狭窄、高血压等心血管疾病的基本病理变化之一。除了血管中膜SMCs外，血管Sca-1+祖细胞也参与其中，但调控机制尚不清楚。我们前期发现，内膜新生过程中ABI3BP表达上调与Sca-1+祖细胞数目增多存在时空关联，同时ABI3BP诱导血管平滑肌细胞（SMCs）SDF-1ɑ表达上调，为Sca-1+祖细胞定向迁移提供路标，此外ABI3BP通过Smad3信号通路促进血管外膜Sca-1+祖细胞分化为SMCs，但二者关联及其机制不明。据此提出“ABI3BP通过差异化调节中膜SMCs和血管外膜Sca-1+祖细胞功能影响新生内膜形成”科学假说。为此，本项目以ABI3BP调节中膜SMCs和血管外膜Sca-1+祖细胞差异性作用为切入点，探索ABI3BP介导的中膜SDF-1ɑ信号与血管外膜Sca-1+祖细胞功能变化的关联特征，以期为临床解决基于血管重构的血管疾病提供新的治疗靶点。

The basic pathological features of hypertension and PCI postoperative restenosis include vascular remodeling. In addition to smooth muscle cells （SMCs）, Sca-1+ progenitor cells are also involved in the process, but the regulatory mechanism remains unclear. In the previous study, we found the up-regulation of ABI3BP during neointimal formation was spatiotemporally correlated with the increase of Sca-1+ progenitor cells，which subsequently induce SMCs SDF-1α expression to be a signpost of Sca-1+ progenitor migration. At the same time, ABI3BP promotes Sca-1+ progenitor differentiation through Smad3 signaling, But the related mechanism is unclear. Therefore, a scientific hypothesis is proposed that “ABI3BP affects neointima formation through differential regulation of the SMCs and vascular Sca-1+ progenitor cells”. This study focuses on the differential effect of ABI3BP in regulating SMCs and adventitia Sca-1+ progenitor cells, to explore the correlation between ABI3BP-mediated SDF-1ɑ signaling and changes of Sca-1+ progenitor cell function . Finally, it hopes to provide a new therapeutic target for clinically solving vascular diseases based on vascular remodeling.