Emodin inhibits macrophage classical activation [Control-LPS-IFNg-Emodin]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE73310 | GEO | 2016/01/02
SECONDARY ACCESSION(S): PRJNA296574
REPOSITORIES: GEO
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Project description:In order to fully characterize emodin's effects on macrophage activation, peritoneal macrophages were stimulated with LPS+IFNg with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IFNg/LPS induced changes in a large percentage of responsive genes (31%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M1 macrophage activation including: TNF, IL6, IL1b, iNOS, MMP2, and MMP9. Three-condition, one-color experiment: Vehicle control, LPS-IFNg or LPS-IFNg-Emodin treated periferal WBC PMN samples: 4 biological replicates each.
2016-07-04 | E-GEOD-73310 | biostudies-arrayexpress
Project description:In order to fully characterize emodin's effects on macrophage alternative activation, peritoneal macrophages were stimulated with IL4 with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IL4 induced changes in a large percentage of genes (60%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M2 macrophage activation including: Arg1, Chi3l3, and CD206.
2016-01-02 | GSE73309 | GEO
Project description:In order to fully characterize emodin's effects on macrophage alternative activation, peritoneal macrophages were stimulated with IL4 with or without emodin and gene expression was analyzed using a whole genome microarray. Emodin significantly attenuated the IL4 induced changes in a large percentage of genes (60%) through inhibiting multiple signaling pathways. RT-qPCR was used to confirm the results in several genes associated with M2 macrophage activation including: Arg1, Chi3l3, and CD206. Three-condition, one-color experiment: Vehicle control, IL4 or IL4-Emodin treated periferal WBC PMN samples: 4 biological replicates each.
2016-07-04 | E-GEOD-73309 | biostudies-arrayexpress
Project description:Emodin inhibits macrophage classical activation [Control-LPS-IFNg-Emodin]
| PRJNA296574 | ENA
Project description:microRNA (miRNA), recently identified, non-coding, small RNA, are emerging as key regulators in homeostasis of the immune system. Therefore, aberrant expression of miRNA may be linked to immune dysfunction, such as in chronic inflammation and autoimmunity. In this study, we investigated the potential role of miRNA in estrogen-mediated regulation of innate immune responses, as indicated by upregulation of LPS-induced IFNg, inducible nitric oxide synthase (iNOS), and nitric oxide in splenic lymphocytes from estrogen-treated mice. We found that miR-146a, a negative regulator of Toll-like receptor (TLR) signaling, was decreased in freshly-isolated splenic lymphocytes from estrogen-treated mice compared to placebo controls. Increasing the activity of miR-146a significantly inhibited LPS-induced IFNg and iNOS expression in mouse splenic lymphocytes. Further, miRNA microarray and Real-time RT-PCR analysis revealed that estrogen selectively upregulates/downregulates the expression of miRNA in mouse splenic lymphocytes. miR-223, which is highly upregulated by estrogen, regulates LPS-induced IFNg, but not iNOS or nitric oxide in splenic lymphocytes. Inhibition of miR-223 activity decreased LPS-induced IFNg in splenic lymphocytes from estrogen-treated mice. Our data are the first demonstrating selective regulation of miRNA expression in immune cells by estrogen and are indicative of an important role of miRNA in estrogen-mediated immune regulation. Keywords: microRNAs, estrogen, splenic lymphocytes, TLR4 signaling, mouse Total RNAs were isolated from freshly-isolated splenic lymphocytes from 2 pairs of placebo-and estrogen-treated mice
2008-12-04 | E-GEOD-11197 | biostudies-arrayexpress
Project description:Emodin inhibits macrophage alernative activation
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Project description:microRNA (miRNA), recently identified, non-coding, small RNA, are emerging as key regulators in homeostasis of the immune system. Therefore, aberrant expression of miRNA may be linked to immune dysfunction, such as in chronic inflammation and autoimmunity. In this study, we investigated the potential role of miRNA in estrogen-mediated regulation of innate immune responses, as indicated by upregulation of LPS-induced IFNg, inducible nitric oxide synthase (iNOS), and nitric oxide in splenic lymphocytes from estrogen-treated mice. We found that miR-146a, a negative regulator of Toll-like receptor (TLR) signaling, was decreased in freshly-isolated splenic lymphocytes from estrogen-treated mice compared to placebo controls. Increasing the activity of miR-146a significantly inhibited LPS-induced IFNg and iNOS expression in mouse splenic lymphocytes. Further, miRNA microarray and Real-time RT-PCR analysis revealed that estrogen selectively upregulates/downregulates the expression of miRNA in mouse splenic lymphocytes. miR-223, which is highly upregulated by estrogen, regulates LPS-induced IFNg, but not iNOS or nitric oxide in splenic lymphocytes. Inhibition of miR-223 activity decreased LPS-induced IFNg in splenic lymphocytes from estrogen-treated mice. Our data are the first demonstrating selective regulation of miRNA expression in immune cells by estrogen and are indicative of an important role of miRNA in estrogen-mediated immune regulation. Keywords: microRNAs, estrogen, splenic lymphocytes, TLR4 signaling, mouse
2008-12-05 | GSE11197 | GEO
Project description:Cervical cancer is one of the most common cancers in women worldwide. The role of HPV in cervical cancer is well studied, however, the underlying mechanism promoting cervical tumorigenesis is still not fully understood. Recently, emodin was shown to induce cell cycle arrest, induction of differentiation, downregulation of TGF β signaling pathway and apoptosis in cervical cancer cell lines. Further, recent studies have shown the role of miRNAs in mediating abnormal regulatory mechanisms leading to the pathogenesis of cervical cancer and large scale miRNA profiling studies have examined the use of miRNAs as cervical cancer diagnostic markers. However, to date, there is no study being performed to analyze the changes in miRNAs following emodin treatment to determine whether emodin mediates its effects by regulating the expression of miRNAs. Therefore, the aim of the current study is to perform miRNA profiling in cervical cancer cells following emodin treatment and to analyze the roles of differentially expressed miRNAs in regulating the pathogenesis and treatment of cervical cancer.
2022-06-30 | GSE135699 | GEO
Project description:Long non-coding RNAs (lncRNAs) reportedly contribute to disease pathogenesis and drug treatment effects. Both emodin and dexamethasone (DEX) have been used for the treatment of severe acute pancreatitis-associated acute lung injury (SAP-ALI). However, lncRNA regulation networks related to SAP-ALI pathogenesis and drug treatment are unreported. In this study, lncRNAs and mRNAs in the lung tissue of SAP-ALI and control rats, with or without drug treatment (emodin or DEX), were assessed by RNA sequencing. Results showed that both emodin and DEX were therapeutic for SAP-ALI and that mRNA and lncRNA levels differed between untreated and treated SAP-ALI rats. Gene expression profile relationships for emodin treated and control rats were higher than DEX treated and untreated animals. By comparison of control and SAP-ALI animals, more upregulated than downregulated mRNAs and lncRNAs were observed with emodin treatment. For DEX treatment, more downregulated than upregulated mRNAs and lncRNAs were observed. Functional analysis demonstrated both upregulated mRNA and co-expressed genes with upregulated lncRNAs were enriched in inflammatory and immune response pathways. Further, emodin associated lncRNAs and mRNAs co-expressed modules were different from those associated with DEX. Quantitative polymerase chain reaction demonstrates that selected lncRNA and mRNA co-expressed modules were different in the lung tissue of emodin and DEX treated rats. Also, emodin had different effects compared to DEX on the co-expression network of lncRNAs Rn60_7_1164.1 and AABR07062477.2 for the blue lncRNA module and Nrp1 for the green mRNA module. In conclusion, this study provides evidence that emodin may be a suitable alternative or complementary medicine for treatment of SAP-ALI.
2021-01-03 | GSE151572 | GEO
Project description:Heterogeneous nuclear ribonucleoprotein A2B1 (HNRNPA2B1) is a well known RNA binding protein but the mechanisms by which it contributes to innate immune gene regulation is poorly understood. Here we report that HNRNPA2B1 functions in macrophages to regulate IFNG signaling through alternative splicing of the IFNG receptor. Specific deletion of HNRNPA2B1 in macrophages using our newly developed conditional mice crossed to LysMCre resulted in altered cytokine responses in both an endotoxic shock model and following Salmonella infection. Interestingly, while HNRNPA2B1 can function as a viability gene, we observed increased macrophage and neutrophil numbers in the KO mice following LPS induced endotoxic shock. HNRNPA2B1 KO mice were more susceptible to Salmonella and Mycobacterium Tuberculosis infections and failed to effectively clear the pathogens. Mechanistically, loss of HNRNPA2B1 resulted in an increase in No-GO transcripts of the IFNG receptor (Ifngr) leading to lower expression of the receptor at the cell surface impacting the downstream IFNG signaling cascade. Collectively, our data highlights an important role for HNRNPA2B1 in regulating IFNG signaling in macrophages.
2024-09-30 | GSE243269 | GEO