Fosl1 is vital to heart regeneration upon apex resection in adult Xenopus tropicalis.

Cardiovascular disease is the leading cause of death in the world due to losing regenerative capacity in the adult heart. Frogs possess remarkable capacities to regenerate multiple organs, including spinal cord, tail, and limb, but the response to heart injury and the underlying molecular mechanism remains largely unclear. Here we demonstrated that cardiomyocyte proliferation greatly contributes to heart regeneration in adult X. tropicalis upon apex resection. Using RNA-seq and qPCR, we found that the expression of Fos-like antigen 1 (Fosl1) was dramatically upregulated in early stage of heart injury. To study Fosl1 function in heart regeneration, its expression was modulated in vitro and in vivo. Overexpression of X. tropicalis Fosl1 significantly promoted the proliferation of cardiomyocyte cell line H9c2. Consistently, endogenous Fosl1 knockdown suppressed the proliferation of H9c2 cells and primary cardiomyocytes isolated from neonatal mice. Taking use of a cardiomyocyte-specific dominant-negative approach, we show that blocking Fosl1 function leads to defects in cardiomyocyte proliferation during X. tropicalis heart regeneration. We further show that knockdown of Fosl1 can suppress the capacity of heart regeneration in neonatal mice, but overexpression of Fosl1 can improve the cardiac function in adult mouse upon myocardium infarction. Co-immunoprecipitation, luciferase reporter, and ChIP analysis reveal that Fosl1 interacts with JunB and promotes the expression of Cyclin-T1 (Ccnt1) during heart regeneration. In conclusion, we demonstrated that Fosl1 plays an essential role in cardiomyocyte proliferation and heart regeneration in vertebrates, at least in part, through interaction with JunB, thereby promoting expression of cell cycle regulators including Ccnt1.

Natural Self-Confined Structure Effectively Suppressing Volume Expansion toward Advanced Lithium Storage.

Volume expansion hinders conversion-type transition-metal oxides (TMOs) as potential anode candidates for high-capacity lithium-ion batteries. While nanostructuring and nanosizing have been employed to improve the cycling stability of TMOs, we show here that both high initial Coulombic efficiency (ICE) and stable cycling reversibility are achieved in the layered compound Li0.9Nb0.9Mo1.1O6 (L0.9NMO) by inherent properties of the bulk crystal structure. In this model, MoO6 octahedra as active centers react with lithium ions and endow capacity, while a grid composed of NbO6 octahedra effectively suppresses the volume expansion, enhances the conductivity, and supports the structural skeleton from collapse. As a result, bulk L0.9NMO not only delivers a high discharge capacity of 1128 mA h g-1 at 100 mA g-1 with a considerable ICE of 87% but also exhibits long cycling stability and good rate performance (339 mA h g-1 after 500 cycles at 1 A g-1 with an average Coulombic efficiency approaching 100%). The self-confined structure provides a competitive strategy for stable conversion-type lithium storage.