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  • Open Access

    ARTICLE

    miRNA-148b-3p targeting SOCS3 inhibits macrophage M2 polarization by JAK2/STAT3 pathway in immune thrombocytopenia

    YANG YANG, LIJUAN FU, CHUNMEI CHEN, MEIWEI HU

    BIOCELL, Vol.46, No.5, pp. 1319-1328, 2022, DOI:10.32604/biocell.2022.015760 - 06 January 2022

    Abstract Aberrant expression of miRNAs is significantly correlated with the occurrence of immune thrombocytopenic purpura (ITP). The immune imbalance of M1/M2 macrophage contributes to the development of ITP. However, the role of miR-148b-3p in macrophage phenotype imbalance remains unknown in ITP. In this study, we aimed to explore whether miR-148b-3p inhibits M2 macrophage polarization in ITP and to investigate the underlying mechanism. Peripheral blood from 22 ITP patients were collected, and real-time PCR confirmed that miR-148b-3p was up-regulated and Western blot analyses detected the expression of SOCS3 was down-regulated. Subsequent dual-luciferase reporter gene assay indicated that More >

  • Open Access

    ARTICLE

    Aberrant DNA methylation of the promoters of JAK2 and SOCS3 in juvenile systemic lupus erythematosus

    Mahsa Keshavarz-Fathi1,2,3, Golshid Sanati3,4,5, Maryam Sadr3, Bahareh Mohebbi3, Vahid Ziaee6,7, Nima Rezaei3,5,8

    European Cytokine Network, Vol.32, No.3, pp. 48-54, 2021, DOI:10.1684/ecn.2021.0469

    Abstract Cytokine dysregulation is one of the important hallmarks of systemic lupus erythematosus (SLE) in both pediatric and adult patients. Owing to the substantial role of Janus kinase (JAK) and suppressor of cytokine signaling (SOCS) in cytokine signaling, we compared the methylation status of the promoter of JAK2 and SOCS3 between patients with JSLE and healthy controls. Methods: Peripheral blood samples were obtained from patients with JSLE and healthy controls. The promoter methylation was assessed by using the bisulfite conversion system and real-time quantitative multiplex methylation-specific PCR (QM-MSP). Results: The methylation assessments were performed on the… More >

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