文獻(xiàn)引用抗體：bs-7656R

ATAD5 Rabbit pAb | WB

作者單位：四川大學(xué)華西醫(yī)院

摘要：The mineral dust-induced gene (MDIG) comprises a conserved JmjC domain and has the ability to demethylate histone H3 lysine 9 trimethylation (H3K9me3). Previous studies have indicated the significance of MDIG in promoting cell proliferation by modulating cell-cycle transition. However, its involvement in liver regeneration has not been extensively investigated. In this study, we generated mice with liver-specific knockout of MDIG and applied partial hepatectomy or carbon tetrachloride mouse models to investigate the biological contribution of MDIG in liver regeneration. The MDIG levels showed initial upregulation followed by downregulation as the recovery progressed. Genetic MDIG deficiency resulted in dramatically impaired liver regeneration and delayed cell cycle progression. However, the MDIG-deleted liver was eventually restored over a long latency. RNA-seq analysis revealed Myc as a crucial effector downstream of MDIG. However, ATAC-seq identified the reduced chromatin accessibility of OTX2 locus in MDIG-ablated regenerating liver, with unaltered chromatin accessibility of Myc locus. Mechanistically, MDIG altered chromatin accessibility to allow transcription by demethylating H3K9me3 at the OTX2 promoter region. As a consequence, the transcription factor OTX2 binding at the Myc promoter region was decreased in MDIG-deficient hepatocytes, which in turn repressed Myc expression. Reciprocally, Myc enhanced MDIG expression by regulating MDIG promoter activity, forming a positive feedback loop to sustain hepatocyte proliferation. Altogether, our results prove the essential role of MDIG in facilitating liver regeneration via regulating histone methylation to alter chromatin accessibility and provide valuable insights into the epi-transcriptomic regulation during liver regeneration.

bsk12001; IFN-γ ELISA KIT | ELISA

bsk12002; TNF-α ELISA KIT | ELISA

bsk12016; IL-2 ELISA KIT | ELISA

bsk12017; IL-12p70 ELISA KIT | ELISA

bs-0081R; Caspase-3 Rabbit pAb | WB

bs-0664R; HMGB1 Rabbit pAb | WB

bs-0784R; IFNB1 Rabbit pAb | WB

bs-8766R; HAVCR2/TIM-3 Rabbit pAb | WB

bs-9278R; phospho-IRF3 (Ser386) Rabbit pAb | WB

bs-41373R; GAPDH Rabbit pAb | WB

作者單位：南方醫(yī)科大學(xué)附屬第十醫(yī)院

IL-6 Rabbit pAb | IHC

作者單位：四川大學(xué)生物質(zhì)科學(xué)與工程學(xué)院、成都大三創(chuàng)新醫(yī)療科技有限公司、重慶醫(yī)科大學(xué)附屬第一醫(yī)院泌尿外科

摘要：Hydrophilic lubricant coatings with antifouling properties are commercially applied to urological devices, such as ureteral stents (USs), to inhibit biofilm formation and reduce the likelihood of infectious encrustation. However, their long-term effectiveness is limited due to the lack of active and precise antibacterial activity. Herein, this work reports a hydrophilic lubricant (defined as SA-PU/PVP) coating with smart urease-responsive antibiotic release functionality, achieved by incorporating the antibiotic sulfanilamide-conjugated polyurethane (SA-PU) polymers into a commercial lubricant coating agent containing hydrophilic polyvinylpyrrolidone (PVP). During the initial implantation period, the hydrophilic PVP chains rapidly absorb urine on the coating interface, forming a lubricating layer with the desired antifouling activities that reduce the attachment of host proteins, bacteria, and urate crystals by over 90%. As time progresses and the bacteria proliferates and produces urease, the urease enzymatically degrades the urea linkages in the SA-PU/PVP coating, actively releasing SA antibiotics on demand to prevent biofilm formation and encrustation. Benefiting from this synergistic antifouling and smart antibacterial activities, the SA-PU/PVP-coated US exhibits superior performance in preventing infectious encrustation in a porcine model over a 7-week period, surpassing the effectiveness of a commercial hydrophilic lubricant US. This coating strategy offers a practical solution for inhibiting urological device-associated complications.

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