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Nuclear receptor coactivator 6 is a critical regulator of NLRP3 inflammasome activation and gouty arthritis

Cellular & Molecular Immunology 2024年第3期21卷 227-244页

作者： Kang-Gu Lee Bong-ki.Hong Saseong Lee Naeun Lee Seung-Whan ki. donghyun ki. Wan-Uk ki. Center for Integrative Rheumatoid Transcriptomics and Dynamics The Catholic University of KoreaSeoul 06591Republic of Korea Department of Biomedicine&Health Sciences The Catholic University of KoreaSeoul 06591Republic of Korea Department of Pharmacology Asan Medical CenterUniversity of Ulsan College of MedicineSeoul 05505Republic of Korea Bio-Medical Institute of Technology University of UlsanSeoul 05505Republic of Korea Department of Microbiology and Immunology Seoul National University College of MedicineSeoul 03080Republic of Korea Institute of Infectious Diseases Seoul National University College of MedicineSeoul 03080Republic of Korea Division of Rheumatology Department of Internal MedicineThe Catholic University of KoreaSeoul 06591Republic of Korea

Transcriptional coactivators regulate the rate of gene expression in the *** receptor coactivator 6(NCOA6),a coactivator,has been implicated in embryonic development,metabolism,and cancer pathogenesis,but its role in innate immunity and inflammatory diseases remains ***,we demonstrated that NCOA6 was expressed in monocytes and macrophages and that its level was increased under proinflammatory ***,nuclear NCOA6 was found to translocate to the cytoplasm in activated monocytes and then become incorporated into the inflammasome with NLRP3 and ASC,forming cytoplasmic ***,NCOA6 associated with the ATP hydrolysis motifs in the NACHT domain of NLRP3,promoting the oligomerization of NLRP3 and ASC and thereby instigating the production of IL-1βand active *** note,Ncoa6 deficiency markedly inhibited NLRP3 hyperactivation caused by the Nlrp3^(R258W) gain-of-function mutation in *** ablation of Ncoa6 substantially attenuated the severity of two NLRP3-dependent diseases,folic-induced acute tubular necrosis and crystal-induced arthritis,in *** with these findings,NCOA6 was highly expressed in macrophages derived from gout patients,and NCOA6-positive macrophages were significantly enriched in gout macrophages according to the transcriptome profiling ***,NCOA6 is a critical regulator of NLRP3 inflammasome activation and is therefore a promising target for NLRP3-dependent diseases,including gout.

关键词： Nuclear receptor coactivator 6 Nuclear-to-cytoplasmic translocation NLRP3 inflammasome NACHT domain Gouty arthritis

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CORM-2-entrapped ultradeformable liposomes ameliorate acute ski. inflammation in an ear edema model via effective CO delivery

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Acta Pharmaceutica Sinica B 2020年第12期10卷 2362-2373,2440页

作者： Gwan-Yeong Lee Alam Zeb Eun-Hye ki. Beomseon Suh Young-Jun Shin donghyun ki. Kyoung-Won ki. Yeong-Hwan Choe Ho-Ik Choi Cheol-Ho Lee Omer Salman Qureshi In-Bo Han Sun-Young Chang Ok-Nam Bae Jin-ki.ki. College of Pharmacy Institute of Pharmaceutical Science and TechnologyHanyang UniversityAnsan 15588Republic of Korea Riphah Institute of Pharmaceutical Sciences Riphah International UniversityIslamabad 44000Pakistan Department of Pharmacy Forman Christian CollegeLahore 54600Pakistan Department of Neurosurgery CHA Bundang Medical CenterSchool of MedicineCHA UniversitySeongnam 13496Republic of Korea College of Pharmacy Ajou UniversitySuwon 16499Republic of Korea

The short release half-life of carbon monoxide(CO)is a major obstacle to the effective therapeutic use of carbon monoxide-releasing molecule-2(CORM-2).The potential of CORM-2-entrapped ultradeformable liposomes(CORM-2-UDLs)to enhance the release half-life of CO and alleviate ski. inflammation was investigated in the present ***-2-UDLs were prepared by using soy phosphatidylcholine to form lipid bilayers and Tween 80 as an edge *** deformability of CORM-2-UDLs was measured and compared with that of conventional liposomes by passing formulations through a filter device at a constant *** release profile of CO from CORM-2-UDLs was evaluated by myoglobin *** vitro and in vivo anti-inflammatory effects of CORM-2-UDLs were assessed in lipopolysaccharide-stimulated macrophages and TPA-induced ear edema model,*** deformability of the optimized CORM-2-UDLs was 2.3 times higher than conventional ***-2-UDLs significantly prolonged the release half-life of CO from 30 s in a CORM-2 solution to 21.6 ***-2-UDLs demonstrated in vitro anti-inflammatory activity by decreasing nitrite production and pro-inflammatory cytoki.e ***,CORM-2-UDLs successfully ameliorated ski. inflammation by reducing ear edema,pathological scores,neutrophil accumulation,and inflammatory cytoki.es *** results demonstrate that CORM-2-UDLs could be used as promising therapeutics against acute ski. inflammation.

关键词： Carbon monoxide CORM-2 Anti-inflammatory effect Ultradeformable liposomes Ski. inflammation Ear edema

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