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Dihydroartemisinin beneficially regulates splenic immune cell heterogeneity through the SOD3-JNK-ap-1 axis

Science China(Life Sciences) 2022年第8期65卷 1636-1654页

作者： Yiwei Zhang Qilong Li Ning Jiang Ziwei Su Quan Yuan Lei Lv Xiaoyu Sang Ran Chen Ying Feng Qijun Chen Key Laboratory of Livestock Infectious Diseases in Northeast China Ministry of EducationKey Laboratory of ZoonosisCollege of Animal Science and Veterinary MedicineShenyang Agricultural UniversityShenyang 110866China Research Unit for Pathogenic Mechanisms of Zoonotic Parasites Chinese Academy of Medical SciencesShenyang 110866China

The immunomodulatory potential of dihydroartemisinin(DHA) has recently been highlighted;however, the potential mechanism remains to be clarified. Single-cell RNA sequencing was explored in combination with cellular and biochemical approaches to elucidate the immunomodulatory mechanisms of DHA. In this study, we found that DHA induced both spleen enlargement and rearrangement of splenic immune cell subsets in mice. It was revealed that DHA promoted the reversible expansion of effective regulatory T cells and interferon-γ^(+)cytotoxic CD8^(+)T cells in the spleen via induction of superoxide dismutase 3(SOD3) expression and increased phosphorylation of c-Jun N-terminal kinases(JNK) and its downstream activator protein 1(ap-1) transcription factors. Further, SOD3 knockout mice were resistant to the regulatory effect of DHA. Thus, DHA,through the activation of the SOD3-JNK-ap-1 axis, beneficially regulated immune cell heterogeneity and splenic immune cell homeostasis to treat autoimmune diseases.

关键词： dihydroartemisinin immunomodulatory activity single-cell RNA sequencing ap-1 transcription factor SOD3

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Forskolin and Phorbol 12-myristate 13-acetate modulates the expression pattern of ap-1 factors and cell cycle regulators in estrogen-responsive MCF-7 cells

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Genes & Diseases 2019年第2期6卷 159-166页

作者： R.L.Babu M.Naveen Kumar Rajeshwari H.Patil K.M.Kiran Kumar K.S.Devaraju Govindarajan T.Ramesh S.Chidananda Sharma Department of Bioinformatics and Biotechnology Akkamahadevi Women’s UniversityJnanashakthi CampusVijayapura586108KarnatakaIndia Department of Microbiology and Biotechnology Bangalore UniversityJnana BharathiBengaluru560056KarnatakaIndia Department of Biochemistry Karnatak UniversityDharwad580003KarnatakaIndia Department of Biology Center for Biotechnology and Biomedical SciencesNorfolk State UniversityNorfolkVAUSA

Activator protein-1(ap-1)transcription factor is a key component of many signal transduction pathways involved in the regulation of cellular processes and controls rapid responses of mammalian cells when exposed to the variety of *** phorbol 12-myristate 13-acetate and Forskolin(Fo)are well-known kinase activators/stimulators of Protein Kinase C(PKC)and Protein Kinase A(PKA)***,these kinases are found to be present in transitional points of many cell signaling pathways,especially those involved in *** stimulating effect of PKC and PKA on the expression of ap-1 factors in MCF-7 breast cell proliferation is not well ***,the role of PKC by PMA treatment and the role of PKA by using Fo in MCF-7 cells is ***,cells treated with PMA showed increased cell proliferation,while Fo had no effect,but inhibited the PMA induced *** RT-PCR results showed the PMA induced c-Jun,c-Fos and Fra-1 expressions compared to control and ***,Fo in combination with PMA,inhibit the PMA induced above mRNA expressions where Fo alone has no *** blot studies validated the c-Jun expressions in PMA treated MCF-7 ***,PMA increases the mRNA expression of Cyclin-E1,Cyclin-D1,and CDK-4,whereas Fo decreases their ***,mitogenic effect of PMA and inhibitory action of Fo on MCF-7 cells is probably enhanced via activation of ap-1 factors and concomitant action of cell cycle regulators in the downstream singling cascade.

关键词： ap-1 transcription factor Cell cycle Forskolin MCF-7 cells Phorbol esters

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Jianpi Qinghua Formula Alleviates Diabetic Myocardial Injury Through Inhibiting JunB/c-Fos Expression

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Current Medical Science 2024年第1期44卷 144-155页

作者： Lin WANG Qing-guang CHEN Hao LU Department of Endocrinology Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese MedicineShanghai 201203China Department of Traditional Chinese Medicine Naval Medical UniversityShanghai 200433China

Objective Diabetic cardiomyopathy(DCM)represents a substantial risk factor for heart failure and increased mortality in individuals afflicted with diabetes mellitus(DM).DCM typically manifests as myocardial fibrosis,myocardial hypertrophy,and impaired left ventricular diastolic *** the clinical utility of the Jianpi Qinghua(JPQH)formula has been established in treating diabetes and insulin resistance,its potential efficacy in alleviating diabetic cardiomyopathy remains *** study aims to investigate the impact and underlying molecular mechanisms of the JPQH formula(JPQHF)in ameliorating myocardial injury in nonobese diabetic rats,specifically focusing on apoptosis and *** Wistar rats were assigned as the normal control group(CON),while Goto-Kakizaki(GK)rats were randomly divided into three groups:DM,DM treated with the JPQHF,and DM treated with metformin(MET).Following a 4-week treatment regimen,various biochemical markers related to glucose metabolism,cardiac function,cardiac morphology,and myocardial ultrastructure in GK rats were *** sequencing was utilized to analyze differential gene expression and identify potential therapeutic *** vitro experiments involved high glucose to induce apoptosis and inflammation in H9c2 *** viability was evaluated using CCK-8 assay,apoptosis was monitored via flow cytometry,and the production of inflammatory cytokines was measured using quantitative real-time PCR(qPCR)and *** expression levels were determined by Western blotting *** investigation also incorporated the use of MapK inhibitors to further elucidate the mechanism at both the transcriptional and protein *** The JPQHF group exhibited significant reductions in interventricular septal thickness at end-systole(IVSs)and left ventricular internal diameter at end-systole and end-diastole(LVIDs and LVIDd).JPQHF effectively suppressed high glucose-induced activation of IL-1βand caspase 3 in

关键词： Jianpi Qinghua formula diabetic cardiomyopathy ap-1 transcription factor apoptosis inflammation

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Identification of differentially expressed genes after partial rat liver ischemia/reperfusion by suppression subtractive hybridization

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World Journal of Gastroenterology 2005年第9期11卷 1303-1316页

作者： Christine Fallsehr Christina Zapletal Michael Kremer Resit Demir Magnus von Knebel Doeberitz Ernst Klar Institute of Molecular Pathology Department of Surgery

AIM: To identify potential diagnostic target genes in early reperfusion periods following warm liver ischemia before irreversible liver damage occurs. METHODS: We used two strategies (SSH suppression subtractive hybridization and hybridization of cDNA arrays) to determine early changes in gene expression profiles in a rat model of partial WI/R, comparing postischemic and adjacent nonischemic liver lobes. Differential gene expression was verified (WI/R; 1 h/2 h) and analyzed in more detail after warm ischemia (1 h) in a reperfusion time kinetics (0, 1, 2 and 6 h) and compared to untreated livers by Northern blot hybridizations. Protein expression was examined on Western blots and by immunohistochemistry for four differentially expressed target genes (Hsp70, Hsp27, Gadd45a and IL-1rI). RESULTS: Thirty-two individual WI/R target genes showing altered RNA levels after confirmation by Northern blot analyzes were identified. Among them, six functionally uncharacteristic expressed sequences and 26 known genes (12 induced in postischemic liver lobes, 14 with higher transcriptional expression in adjacent nonischemic liver lobes). Functional categories of the verified marker genes indicate on the one hand cellular stress and tissue damage but otherwise activation of protective cellular reactions (ap-1 transcription factors, apoptosis related genes, heat shock genes). In order to assign the transcriptional status to the biological relevant protein level we demonstrated that Hsp70, Hsp27, Gadd45a and IL-1rI were clearly up-regulated comparing postischemic and untreated rat livers, suggesting their involvement in the WI/R context. CONCLUSION: This study unveils a WI/R response gene set that will help to explore molecular pathways involved in the tissue damage after WI/R. In addition, these genes especially Hsp70 and Gadd45a might represent promising new candidates indicating WI/R liver damage.

关键词： Organ injury Liver ischemia ap-1 transcription factor Heat shock protein Gadd45A Suppression subtractive hybridization

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