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Mesenchymal stem cells (MSCs) have shown great potential for the treatment of liver injuries, and the therapeutic efficacy greatly depends on their homing to the site of injury. In the present study, we detected significant upregulation of hepatocyte growth factor (HGF) in the serum and liver in mice with acute or chronic liver injury. In vitro study revealed that upregulation of miR-9-5p or miR-221-3p promoted the migration of human MSCs (hMSCs) toward HGF. Moreover, overexpression of miR-9-5p or miR-221-3p promoted hMSC homing to the injured liver and resulted in significantly higher engraftment upon peripheral infusion. hMSCs reduced hepatic necrosis and inflammatory infiltration but showed little effect on extracellular matrix (ECM) deposition. By contrast, hMSCs overexpressing miR-9-5p or miR-221-3p resulted in not only less centrilobular necrosis and venous congestion but also a significant reduction of ECM deposition, leading to obvious improvement of hepatocyte morphology and alleviation of fibrosis around central vein and portal triads. Further studies showed that hMSCs inhibited the activation of hepatic stellate cells (HSCs) but could not decrease the expression of TIMP-1 upon acute injury and the expression of MCP-1 and TIMP-1 upon chronic injury, while hMSCs overexpressing miR-9-5p or miR-221-3p led to further inactivation of HSCs and downregulation of all three fibrogenic and proinflammatory factors TGF-β, MCP-1, and TIMP-1 upon both acute and chronic injuries. Overexpression of miR-9-5p or miR-221-3p significantly downregulated the expression of α-SMA and Col-1α1 in activated human hepatic stellate cell line LX-2, suggesting that miR-9-5p and miR-221-3p may partially contribute to the alleviation of liver injury by preventing HSC activation and collagen expression, shedding light on improving the therapeutic efficacy of hMSCs via microRNA modification. [ABSTRACT FROM AUTHOR]

Prussian blue analogues (PBAs) are promising cathode materials for sodium‐ion batteries (SIBs) due to their tunable chemistry, open channel structure, and low cost. However, excessive crystal water and volume expansion can negatively impact the lifetime of actual SIBs. In this study, a novel iron nitroprusside: Fe[Fe(CN)5NO] (PBN) was synthesized to effectively eliminate the detrimental effects of crystal water on the reversible capacity and cycling stability of PBA materials. Experiments and DFT calculations demonstrated that PBN has lower crystal water and volume expansion compared to Fe[Fe(CN)6] (PB). Also, the N=O bond in PBN significantly reduces the diffusion potential of Na+ in the skeleton. Without any modification, the cathode material exhibited a capacity of up to 148.6 mAh g−1 at 50 mA g−1 as well as maintained 102.9 mAh g−1 after 200 cycles. This work expands our knowledge of the crystal structure of PBA cathode materials and facilitates the rational design of high‐quality PBA cathodes for SIBs. [ABSTRACT FROM AUTHOR]

Transplanted mesenchymal stem cells (MSCs) can significantly aid in repairing spinal cord injuries (SCI) by migrating to and settling at the injury site. However, this process is typically inefficient, as only a small fraction of MSCs successfully reach the target lesion area. During SCI, the increased expression and secretion of hepatocyte growth factor (HGF) act as a chemoattractant that guides MSC migration. Nonetheless, the precise mechanisms by which HGF influences MSC migration are not fully understood. This study focused on unraveling the molecular pathways that drive MSC migration towards the SCI site in response to HGF. It was found that HGF can activate β-catenin signaling in MSCs either by phosphorylating LRP6 or by suppressing GSK3β phosphorylation through the AKT and ERK1/2 pathways, or by enhancing the expression and nuclear translocation of TCF4. This activation leads to elevated Nedd9 expression, which promotes focal adhesion formation and F-actin polymerization, facilitating chemotactic migration. Transplanting MSCs during peak HGF expression in injured tissues substantially improves nerve regeneration, reduces scarring, and enhances hind limb mobility. Additionally, prolonging HGF release can further boost MSC migration and engraftment, thereby amplifying regenerative outcomes. However, inhibiting HGF/Met or interfering with β-catenin or Nedd9 signaling significantly impairs MSC engraftment, obstructing tissue repair and functional recovery. Together, these findings provide a theoretical basis and practical strategy for MSC transplantation therapy in SCI, highlighting the specific molecular mechanisms by which HGF regulates β-catenin signaling in MSCs, ultimately triggering their chemotactic migration., (© The Author(s) 2024. Published by Oxford University Press. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Prussian blue analogues (PBAs) are promising cathode materials for sodium-ion batteries (SIBs) due to their tunable chemistry, open channel structure, and low cost. However, excessive crystal water and volume expansion can negatively impact the lifetime of actual SIBs. In this study, a novel iron nitroprusside: Fe[Fe(CN) 5 NO] (PBN) was synthesized to effectively eliminate the detrimental effects of crystal water on the reversible capacity and cycling stability of PBA materials. Experiments and DFT calculations demonstrated that PBN has lower crystal water and volume expansion compared to Fe[Fe(CN) 6 ] (PB). Also, the N=O bond in PBN significantly reduces the diffusion potential of Na + in the skeleton. Without any modification, the cathode material exhibited a capacity of up to 148.6 mAh g -1 at 50 mA g -1 as well as maintained 102.9 mAh g -1 after 200 cycles. This work expands our knowledge of the crystal structure of PBA cathode materials and facilitates the rational design of high-quality PBA cathodes for SIBs., (© 2023 Wiley-VCH GmbH.)

Objective: To explore the proliferation and apoptosis effects induced by sodium arsenite and arsenic trioxide on human hepatocyte L02 and provide evidence for the paradox effects of arsenic., Methods: Human hepatocyte L02 was treated by a series of concentration of sodium arsenite or arsenic trioxide, respectively. Cytotoxicity were tested by MTT assay and colony formation assay, cellular apoptosis and cell cycle were detected by flow cytometry, chromosomal breakage were measured by micronucleus test and reactive oxygen species level and GSH contents were detected with commercial kits., Results: With the increase of sodium arsenite or arsenic trioxide concentrations, cellular viability, colony formation rate and GSH contents decreased; inhibition of colony formation, cellular apoptotic rate, reactive oxygen species level and frequency of micronuclei increased, and dosed cells were both arrested in G2/M phase of cell cycle., Conclusion: Both sodium arsenite and arsenic trioxide could induce oxidative stress in human hepatocyte L02 and result in chromosomal damage, apoptosis, cell cycle arrest and cellular proliferation inhibition, suggesting that oxidative stress induction might be the common molecular mechanism of malignant transformation induced by sodium arsenite and therapeutic effects exhibited by arsenic trioxide.