Simple synthesis of photoluminescent carbon dots from a marine polysaccharide found in shark cartilage

BACKGROUND: For more than a decade, water-soluble, eco-friendly, biocompatible, and low-toxicity fluorescent nanomaterials have received considerable attention for their numerous in vivo and in vitro applications in biomedical imaging, disease diagnostics, and environmental monitoring. Owing to their tunable photoluminescence properties, carbon-based luminescent nanomaterials have shown great potential in bioimaging, photocatalysis, and biosensing among other applications. RESULTS: Marine environments provide excellent resources for the fabrication of these nanomaterials, because many marine organisms contain interesting trigger organic compounds that can be used as precursors. Herein, we synthesize multi-color emissive carbon dots (CDs) with an intrinsic photoluminescence quantum yield of 20.46%. These nanostructures were achieved through the one-step hydrothermal treatment of marine polysaccharide chondroitin sulfate, obtained from shark cartilage, in aqueous solution. CONCLUSIONS: We successfully demonstrate the low toxicity of our marine resource-derived CDs in zebrafish, and provide an initial assessment of their possible use as a bioimaging agent. Notably, the newly synthesized CDs localize in the intestines of zebrafish larvae, thereby indicating their biocompatibility and potential use as in vivo dyes.

Bone morphogenetic protein signaling governs biliary-driven liver regeneration in zebrafish through tbx2b and id2a.

Upon mild liver injury, new hepatocytes originate from preexisting hepatocytes. However, if hepatocyte proliferation is impaired, a manifestation of severe liver injury, biliary epithelial cells (BECs) contribute to new hepatocytes through BEC dedifferentiation into liver progenitor cells (LPCs), also termed oval cells or hepatoblast-like cells (HB-LCs), and subsequent differentiation into hepatocytes. Despite the identification of several factors regulating BEC dedifferentiation and activation, little is known about factors involved in the regulation of LPC differentiation into hepatocytes during liver regeneration. Using a zebrafish model of near-complete hepatocyte ablation, we show that bone morphogenetic protein (Bmp) signaling is required for BEC conversion to hepatocytes, particularly for LPC differentiation into hepatocytes. We found that severe liver injury led to the up-regulation of genes involved in Bmp signaling, including smad5, tbx2b, and id2a, in the liver. Bmp suppression did not block BEC dedifferentiation into HB-LCs; however, the differentiation of HB-LCs into hepatocytes was impaired due to the maintenance of HB-LCs in an undifferentiated state. Later Bmp suppression did not affect HB-LC differentiation but increased BEC number through proliferation. Notably, smad5, tbx2b, and id2a mutants exhibited similar liver regeneration defects as those observed in Bmp-suppressed livers. Moreover, BMP2 addition promoted the differentiation of a murine LPC line into hepatocytes in vitro. CONCLUSIONS: Bmp signaling regulates BEC-driven liver regeneration through smad5, tbx2b, and id2a: it regulates HB-LC differentiation into hepatocytes through tbx2b and BEC proliferation through id2a; our findings provide insights into promoting innate liver regeneration as a novel therapy. (Hepatology 2017;66:1616-1630).