RESUMO
The role of microRNA (miRNA) in gestational diabetes mellitus has been widely investigated during the last decade. However, the altering effect of miR-6869-5p on immunity and placental microenvironment in gestational diabetes mellitus is largely unknown. In our study, the expression of miR-6869-5p was documented to be significantly decreased in placenta-derived mononuclear macrophages, which was also negatively related to PTPRO. Besides, PTPRO was negatively regulated by miR-6869-5p in placenta-derived mononuclear macrophages. In vitro, miR-6869-5p inhibited macrophage proliferation demonstrated by EdU and CCK-8 experiments. The inflammatory response in macrophages was also significantly inhibited by miR-6869-5p, which could regulate PTPRO as a target documented by luciferase reporter assay. Moreover, miR-6869-5p promoted M2 macrophage polarization and thus restrain inflammation. Accordingly, miR-6869-5p is involved in maintaining placental microenvironment balance by preventing from inflammation and inducing M2 macrophages in gestational diabetes mellitus.
Assuntos
Diabetes Gestacional , MicroRNAs , Diabetes Gestacional/genética , Diabetes Gestacional/metabolismo , Feminino , Humanos , Ativação de Macrófagos , Macrófagos/metabolismo , MicroRNAs/genética , MicroRNAs/metabolismo , Placenta/metabolismo , Gravidez , Proteínas Tirosina Fosfatases Classe 3 Semelhantes a Receptores/metabolismoRESUMO
Chronic myeloid leukemia (CML) is a type of myeloproliferative neoplasm. Aberrant expression of long noncoding RNA highly upregulated in liver cancer (HULC) has been implicated in tumor progression, including CML. This study aimed to investigate the role of HULC in CML. The levels of HULC, miR-150-5p and myeloid cell leukemia 1 (MCL1) were examined by quantitative real-time PCR or western blot assay. Cell counting kit-8 assay was used to detect cell viability and half inhibition concentration. Cell apoptosis was monitored by flow cytometry and western blot. The interaction among HULC, miR-150-5p and MCL1 was validated by dual-luciferase reporter assay. The expression of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) and phosphorylation-AKT was evaluated using western blot assay. HULC and MCL1 were upregulated, whereas miR-150-5p was downregulated in bone marrow mononuclear cells of CML patients and CML cells. HULC overexpression increased imatinib resistance in K562 cells, and HULC depletion enhanced imatinib sensitivity in imatinib-resistant cells (K562-R). Mechanically, HULC was a sponge of miR-150-5p. HULC contributed to imatinib resistance through regulation of miR-150-5p. MCL1 bound to miR-150-5p and reversed the effect of HULC on imatinib resistance. HULC regulated the PI3K/AKT pathway via the miR-150-5p/MCL1 axis. These findings indicated that HULC enhanced imatinib resistance in CML by modulating the miR-150-5p/MCL1 axis, providing a promising biomarker for CML.
Assuntos
Mesilato de Imatinib/farmacologia , Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico , Neoplasias Hepáticas/metabolismo , MicroRNAs/metabolismo , Proteína de Sequência 1 de Leucemia de Células Mieloides/metabolismo , RNA Longo não Codificante/metabolismo , Estudos de Casos e Controles , Linhagem Celular Tumoral , Resistencia a Medicamentos Antineoplásicos , Feminino , Humanos , Células K562 , Leucemia Mielogênica Crônica BCR-ABL Positiva/genética , Leucemia Mielogênica Crônica BCR-ABL Positiva/metabolismo , Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia , Neoplasias Hepáticas/genética , Masculino , MicroRNAs/genética , Pessoa de Meia-Idade , Proteína de Sequência 1 de Leucemia de Células Mieloides/genética , RNA Longo não Codificante/genética , Transdução de Sinais , Regulação para CimaRESUMO
Preeclampsia may affect between 2-8% of all pregnancies. It seriously affects maternal health after pregnancy. This meta-analysis was performed to define the efficacy of vitamins supplementation on the risk of preeclampsia. Potential articles were systematically searched on the databases of Pubmed, Embase and Web of Science up to May 2016. Relative risk (RR) and 95% confidence intervals (95%CIs) were used to analyze the relationship of vitamins supplementation with risk of preeclampsia. Cochran Q test was used to test inter-study heterogeneity. Begg's funnel plot was adopted to assess the potential publication bias. 28 eligible studies were selected. Pooled results indicated that vitamins supplementation could reduce the risk of preeclampsia (RR = 0.74, 95%CI = 0.64-0.86). The studies with non-randomized controlled trial (RCT) analysis also suggested the significant relationship of vitamins supplementation with risk of preeclampsia (RR = 0.60, 95%CI = 0.42-0.85). However, negative results were observed in studies with RCT analysis. Subgroup analysis by vitamin type was performed among the studies with RCT analysis. The results indicated that vitamin D supplementation could significantly reduce the risk of preeclampsia (RR = 0.41, 95%CI = 0.22-0.78). Similar results were observed in the studies with multivitamins supplementation (RR = 0.69, 95%CI = 0.51-0.93). Vitamins supplementation could reduce the onset of preeclampsia.
