YIGSR, DGEA, and VAPG alone were not enough to induce strong, stable VIC adhesion. As a result, 1 mM RGDS was supplemented with these peptides for the remaining studies. Compared to the RGDS only group, DGEA enhanced VIC adhesion, suggesting DGEA can be used to promote VIC adhesion together with RGDS. Our results showed that DGEA promoted collagen secretion and downregulated ALP expression, suggesting that integrin α2β1 binding promotes ECM remodeling and better preserves the quiescent, fibroblastic phenotype of healthy VICs. YIGSR and VAPG reduced αSMA expression of VICs, indicating 67LR binding inhibits myofibroblast activation. Therefore, YIGSR, DGEA and VAPG can regulate VIC phenotypes, and DGEA is potentially beneficial in promoting VIC-mediated ECM remodeling without inducing pathological differentiation. Future work focuses on regulating VIC phenotype and ECM remodeling via adhesion ligands in three dimensional biomimetic hydrogels.
展开▼
机译：单独的YIGSR，DGEA和VAPG不足以引起牢固，稳定的VIC粘附。结果，在剩余的研究中向1 mM RGDS补充了这些肽。与仅RGDS组相比，DGEA增强了VIC的粘附性，表明DGEA可与RGDS一起用于促进VIC的粘附性。我们的结果表明，DGEA促进胶原蛋白分泌并下调ALP表达，这表明整联蛋白α2β1结合可促进ECM重塑并更好地保留健康VIC的静态，成纤维细胞表型。 YIGSR和VAPG降低了VIC的αSMA表达，表明67LR结合抑制了成肌纤维细胞的活化。因此，YIGSR，DGEA和VAPG可以调节VIC表型，而DGEA在促进VIC介导的ECM重塑而不诱导病理分化方面具有潜在的优势。未来的工作重点是通过三维仿生水凝胶中的粘附配体来调节VIC表型和ECM重塑。
展开▼
