Recent advances in the design of cardiovascular materials for biomedical applications.

Biomaterials dominate the field of cardiovascular therapeutics, a multitude of which have been used to repair and replace injured heart tissue. This field has evolved beyond the simple selection of compatible materials and now focuses on the rational design of controlled structures that integrate with the cardiovascular system. However, the compatibility of these materials with the blood presents a major limitation to their clinical application. In this context, surface modification strategies can enhance blood compatibility and several recent advances in this area have emerged. This review summarizes the recent applications of biomaterials in cardiovascular therapies, the improvements in their biocompatibility and the surface modification technologies that have the potential to improve clinical outcomes.

miR-133b Downregulation Reduces Vulnerable Plaque Formation in Mice with AS through Inhibiting Macrophage Immune Responses.

Atherosclerosis (AS) is a chronic inflammatory disease characterized by accumulating deposition of lipids in the arterial intima. Notably, macrophages participate centrally in the pathogenesis of this deadly disease. In this study, we established AS mouse models in order to investigate the effect of microRNA-133b (miR-133b) on vulnerable plaque formation and vascular remodeling in AS and explore the potential functional mechanisms. The expression of miR-133b was altered or the Notch-signaling pathway was blocked in the AS mouse models in order to evaluate the proliferation, migration, and apoptosis of macrophages. It was observed that miR-133b was upregulated in AS, which might target MAML1 to regulate the Notch-signaling pathway. AS mice with downregulated miR-133b or inhibited Notch-signaling pathway presented with a reduced AS plaque area, a decreased positive rate of macrophages, and an increased positive rate of vascular smooth muscle cells. Moreover, Notch-signaling pathway blockade or miR-133b downregulation inhibited the macrophage viability and migration and accelerated the apoptosis. This study provides evidence that downregulated miR-133b expression may inhibit the immune responses of macrophages and attenuate the vulnerable plaque formation and vascular remodeling in AS mice through the MAML1-mediated Notch-signaling pathway, highlighting miR-133b as a novel therapeutic target for AS.

Polarized Distribution of Active Myosin II Regulates Directional Migration of Cultured Olfactory Ensheathing Cells.

Migration of olfactory ensheathing cells (OECs) is critical for development of olfactory system and essential for neural regeneration after OEC transplantation into nerve injury site. However, the molecular mechanisms underlying the regulation of directional migration of OECs remain unclear. In this study, we found that in migrating OECs, phosphorylated myosin light chain (p-MLC, active myosin II) displayed a polarized distribution, with the leading front exhibiting higher than soma and trailing process. Over-expression of GFP-MLC significantly reduced OEC migration. Moreover, decreasing this front-to-rear difference of myosin II activity by the frontal application of a ML-7 (myosin II inhibitors) gradient induced the collapse of leading front and reversed soma translocation of OECs, whereas, increasing this front-to-rear difference of myosin II activity by the rear application of a ML-7 or BDM gradient or the frontal application of a Caly (myosin II activator) gradient accelerated the soma translocation of OECs. Finally, myosin II as a downstream signaling of repulsive factor Slit-2 mediated the reversal of soma translocation induced by Slit-2. Taken together, these results suggest that the polarized distribution of active myosin II regulates the directional migration of OECs during spontaneous migration or upon to extracellular stimulation such as Slit-2.