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GM-CSF-induced Ca_(2.) -activated non-voltage-dependent inwardly rectifying K_+ channel in murine peritoneal exudate macrophages

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chinese Science Bulletin 1997年第11期42卷 947-952页

作者： zhang xiaofeng, feng meifu, {2. {3. and zhou pei’aistate key Laboratory of Biomembrane and membrane biotechnology, chinese academy of sciences,{12.,{13. 1 . In-stitute of Zoology, chinese academy of sciences,{12.,{13. 2.College of Life sciences, Peking University, beijing 100871,{13. State key Laboratory of Biomembrane and membrane {3. Chinese Academy of Sciences Beijing 100080 China

GRANULOCYTE-MACROPHAGE colony-stimulating factor(GM-CSF),a member in the family ofglycoprotein cytokines,can not only act to stimulate proliferation of immature progenitors,butalso enhance differentiated functions of mature effector *** has two kinds of biologicaleffects on mature effector cells,*** effect and indirect *** latter is also

关键词： K+ channel patch clamp GM-CSF macrophage.

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Rapamycin suppresses rheumatoid arthritis fibroblast synovial cell proliferation and induces apoptosis via the AKT/mTORC1 pathway

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Rheumatology & Autoimmunity 2024年第3期4卷 156-164页

作者： Shengxiao zhang Xiaorong Hu Qinyi Su Heyi zhang Ting Cheng Jia Wang Ruomeng {2. Xin Li Ruqi zhang Hongfang Shao caihong Wang xiaofeng Li Department of Rheumatology The Second Hospital of Shanxi Medical UniversityTaiyuanShanxiChina Shanxi Provincial key Laboratory of Rheumatism Immune Microecology TaiyuanShanxiChina key Laboratory of Cellular Physiology at Shanxi Medical University Ministry of EducationTaiyuanShanxiChina Clinical Laboratory Shenzhen Bao'an Maternal and Child Health HospitalShenzhenGuangdongChina Center for Endocrine Metabolism and Immune Diseases Beijing Luhe HospitalCapital Medical UniversityBeijingChina Department of Information Management The Second Hospital of Shanxi Medical UniversityTaiyuanShanxiChina

Background::Rheumatoid arthritis(RA)is an autoimmune disease characterized by the overproliferation of synovial fibroblast-like synoviocytes(FLSs)in the lining,leading to chronic inflammation and progressive joint *** pathogenesis involves lymphocyte infiltration,increased synovial cell proliferation,and impaired cell *** study investigated the effects of rapamycin on RA-FLSs and explored the underlying molecular ***::The optimal drug concentration and time for rapamycin administration were determined using a cell counting kit-8 *** concentration of rapamycin varied from 1 to 2. nmol/*** mRNA expression levels of protein kinase B(AKT),mammalian target of rapamycin(mTOR),B cell lymphoma 2.Bcl-2.,and Bcl-2.associated X protein(Bax)were quantified by real-time polymerase chain *** expression(p-AKT,AKT,p-mTOR,mTOR,pS6 kinase[S6K],S6K,p-4E-binding protein 1[4EBP1],4EBP1,Bcl-2.Bax,caspase 3.caspase 9,cyclin-dependent kinase 2.CDK2.,and CD1)were detected by Western blotting ***::Rapamycin suppresses RA-FLS proliferation and induces apoptosis in a dose-dependent *** significantly elevated the protein expression of Bax(p3.p2.expression(p2.p3.(p2.48)(p2.and CD1(p<0.01).Conclusions::Rapamycin effectively inhibited proliferation and induced apoptosis of RA-FLSs by targeting the AKT/mTORC1 *** findings underscore the potential of rapamycin as a therapeutic candidate for addressing the dysregulated proliferation and inflammatory characteristics of *** clinical investigations are required to validate its application in the management of RA.

关键词： apoptosis mTORC1 rapamycin rheumatoid arthritis synovial fibroblasts

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