Mesenchymal stem cell (MSC)-derived exosomes have been recognized as new candidates for cell-free treatment of various diseases. However, maintaining the retention and stability of exosomes over time in vivo after transplantation is a major challenge in the clinical application of MSC-derived exosomes. Here, we investigated if human placenta-derived MSC-derived exosomes incorporated with chitosan hydrogel could boost the retention and stability of exosomes and further enhance their therapeutic effects. Our results demonstrated that chitosan hydrogel notably increased the stability of proteins and microRNAs in exosomes, as well as augmented the retention of exosomes in vivo as confirmed by Gaussia luciferase imaging. In addition, we assessed endothelium-protective and proangiogenesis abilities of hydrogel-incorporated exosomes in vitro. Meanwhile, we evaluated the therapeutic function of hydrogel-incorporated exosomes in a murine model of hindlimb ischemia. Our data demonstrated that chitosan hydrogel could enhance the retention and stability of exosomes and further augment the therapeutic effects for hindlimb ischemia as revealed by firefly luciferase imaging of angiogenesis. The strategy used in this study may facilitate the development of easy and effective approaches for assessing and enhancing the therapeutic effects of stem cell-derived exosomes.

The weak van der Waals interactions enable ion‐intercalation‐type hosts to be ideal pseudocapacitive materials for energy storage. Here, a methodology for the preparation of hydrated vanadium dioxide nanoribbon (HVO) with moderate transport pathways is proposed. Out of the ordinary, the intercalation pseudocapacitive reaction mechanism is discovered for HVO, which powers high‐rate capacitive charge storage compared with the battery‐type intercalation reaction. The main factor is that the defective crystalline structure provides suitable ambient spacing for rapidly accommodating and transporting cations. As a result, the HVO delivers a fast Zn2+ ion diffusion coefficient and a low Zn2+ diffusion barrier. The electrochemical results with intercalation pseudocapacitance demonstrate a high reversible capacity of 396 mAh g−1 at 0.05 A g−1, and even maintain 88 mAh g−1 at a high current density of 50 A g−1.

BackgroundThere is evidence for inflammation, autophagy, and apoptosis in the ischemic heart. Autophagy is a physiologic process for tissue survival. Apoptosis, on the other hand, is a mechanism that serves to clear the debris in the setting of tissue injury. The balance between autophagy and apoptosis may be important in cell survival and cardiac function.Methods and ResultsWe examined the interplay of inflammation and myocyte autophagy and apoptosis during the ischemic process. We subjected mice to total left coronary artery ligation and studied these animals for up to 4 weeks. The inflammatory (tumor necrosis factor [TNF]‐α, monocyte chemoattractant protein‐1, interleukin‐6, and interleukin‐1β) and autophagic signals (light chain‐3 and beclin‐1) were strongest during the first week and then began to decline. However, the apoptotic signals peaked at week 2 after left coronary artery ligation, and the elevated levels persisted until the end of the fourth week. To elucidate the role of inflammation in the regulation of myocyte autophagy and apoptosis, we administered TNF‐α inhibitor (CAS1049741‐03‐8, Millipore, Burlington, MA) to the mice daily during the first week of myocardial infarction. Anti‐TNF‐α therapy reduced the levels of inflammatory cytokines and the inflammatory cell infiltration in and around the infarct area. However, cardiac function measured by echocardiography (fractional shortening and ejection fraction) worsened with anti‐TNF‐α therapy. More importantly, application of TNF‐α inhibitor markedly inhibited autophagy and promoted myocyte apoptosis in the border zone.ConclusionsThese observations suggest that inflammatory response may be protective in the early stage of the myocardial infarction through stimulation of myocyte autophagy. Anti‐inflammatory treatment early after coronary occlusion may have an adverse effect.

The zinc (Zn)‐ion battery has attracted much attention due to its high safety and environmental protection. At present, the critical issues of the generation of dendrites and the accumulation of dead Zn on the surface will lead to a sharp decline of the battery life. Zn dendrites can be inhibited to some extent by constructing an interface protective coating. However, the existing rigid coating method cannot maintain conformal contact with Zn due to the volume change of Zn deposition and will cause fracture irreversibly during the cycle. Here, a highly self‐adaptable poly(dimethylsiloxane) (PDMS)/TiO2−x coating is developed that can dynamically adapt to volume changes and inhibit dendrites growth. PDMS has high dynamic and self‐adaptability due to the crosslinking of the B–O bond. In addition, the rapid and uniform transfer of Zn2+ is induced by the oxygen‐vacancy‐rich TiO2−x. The assembled cells still achieve 99.6% coulombic efficiency after 700 cycles at a current density of 10 mA cm−2. The adaptive interface coating constructed provides a sufficient guarantee for the stable operation of the Zn anode.

BackgroundBone marrow derived mesenchymal stem cells (bmMSCs) are multipotent cells that can differentiate into diverse cell types, including cardiomyocytes. BmMSC-based transplantation is capable of repairing acute and chronic myocardial infarction. Prior to the transplantation, MSCs are usually induced in vitro by biological reagents and chemicals for directional differentiation. Transforming growth factor beta (TGF-β) is one of the most commonly used biological reagents for induction of cardiomyocyte differentiation of bmMSCs. Previous studies have shown that TGF-β induces senescence in several cell types. However, whether TGF-β affects senescence of bmMSCs has not been elucidated. The goal of this study was to investigate the effect of TGF-β1 on senescence of bmMSCs and the underlying mechanisms.ResultsWe found that TGF-β1 increased activity of senescence-associated-galactosidase (SA-Gal) and production of mitochondrial reactive oxygen species (mtROS) in bmMSCs in a dose-dependent manner. TGF-β1 also significantly decreased expression of superoxide dismutase 2 (SOD2) and Id1, and increased expression of 4-Hydroxynonenal (4-HNE) subunits and p16 in bmMSCs in a dose-dependent manner. Pre-treatment with mtROS inhibitor acetyl-L-carnitine (ALCAR, 0.1 mM) significantly inhibited TGF-β1-induced mtROS production and SA-Gal activity.ConclusionTGF-β1 can induce senescence of bmMSCs, which at least partially depends on mtROS production.