The regulatory role of IL-6R in hepatitis B-associated fibrosis and cirrhosis

This study investigated the expression and regulation of IL-6R in hepatitis B-associated moderate hepatic fibrosis and cirrhosis. Liver tissues, peripheral blood monocytes (PBMs) and serum were collected from 26 hepatitis B patients with liver fibrosis and 35 hepatitis B patients with liver cirrhosis. The levels of Il-6r mRNA expression in these samples were examined by quantitative real-time PCR and IL-6R protein levels were analyzed by western blot and ELISA. MiRNAs that regulate IL-6R expression were predicted by bioinformatics analysis, and validated by dual luciferase reporter assay. Compared with the hepatic fibrosis group, IL-6R was significantly upregulated at both mRNA and protein levels in liver tissues, PBMs and serum samples from the hepatic cirrhosis group (P<0.05). The 3′UTR of Il-6r mRNA was predicted to contain a miR-30b binding site and IL-6R was identified as a possible target of miR-30b. MiR-30b expression was significantly downregulated in samples from hepatic cirrhosis patients compared with hepatic fibrosis patients (P<0.05). In conclusion, IL-6R was upregulated while miR-30b was decreased in patients with liver cirrhosis. The miR-30 can directly regulate the expression of IL-6R.

The variation and significance of plasma hs-CRP,IL-6 and sIL-6R levels in coronary heart disease patients / 西安交通大学学报(医学版)

Objective To investigate the relationship of high sensitivity C reactive protein (hs-CRP), interleukin-6 (IL-6)and soluble IL-6 receptor (sIL-6R)with the severity of clinical symptoms and coronary artery lesions in coronary heart disease (CHD)patients.Methods A total of 522 CHD patients were recruited and divided into three groups:stable angina pectoris (SAP),unstable angina pectoris (UAP)and acute myocardial infarction (AMI)groups.Another 102 healthy individuals served as normal controls (NCs).We calculated Gensini score according to the result of coronary angiography (CAG),collected clinical data and compared the groups. Multiple linear regression analysis was used to investigate the relationship of hs-CRP,IL-6 and sIL-6 R with Gensini score.Results The plasma hs-CRP,IL-6 levels were significantly higher and sIL-6R level was signficantly lower in SAP,UAP and AMI groups than in NC group (P<0 .0 5 ).There was a positive correlation between IL-6 level and Gensini score but a negative correlation between sIL-6 R and Gensini score presented by multiple linear regression analysis (P<0.05 ).Conclusion In CHD patients,plasma hs-CRP,IL-6 and sIL-6R levels are significantly related to the severity of clinical manifestations and coronary artery stenosis.These indicators may help predict the severity of CHD.

Interleukin-1beta Modulates Proliferation, Interleukin-6 and Interleukin Receptor Expression in PC-3 and DU-145 Prostatic Cancer Cells / 대한비뇨기과학회지

Purpose: IL-1 is a multifunctional proinflammatory cytokine. As the proliferative effects of IL-6 and IL-6 receptor expressions on prostatic cancer cells in response to IL-1 have not been determined, the effects of IL-1 on prostatic cancer cell lines were investigated. Materials and Methods: PC-3 and DU-145 cells were cultured in RPMI-1640 medium containing 10% fetal bovine serum. Cell cultures were supplemented with various concentrations of IL-1 (0, 1, 10, 20 and 40ng/ml), and the MMT growth assay performed. PC-3 and DU-145 cells were treated for 2, 4, 8, 12 and 24 h both with and without IL-1. IL-6 and IL-6 receptor (IL-6R) mRNA expressions were investigated using RT-PCR, and the IL-6 levels in cultured supernatant measured by ELISA. Results: The viability of both PC-3 and DU-145 cells decreased after IL-1 treatment (10, 20 and 40ng/mul). With 40ng/ml the IL-1, IL-6 and IL-6RmRNA expressions were lower in PC-3 cells, but unchanged in DU-145 cells, whereas the IL-6 protein production was higher in both PC-3 and DU-145 cells. Conclusions: IL-1 inhibited the proliferation of both PC-3 and DU145 cells. In the PC-3 cells, IL-1 decreased the expressions of IL-6 and IL-6R mRNA, but paradoxically increased the IL-6 production. In the DU-145 cells, IL-1 treatment did not affect the IL-6 or IL-6R mRNA expressions, but the IL-6 production was increased. This discrepancy between IL-1-induced IL-6 mRNA and protein production may be mediated by modification to the protein synthesis or an increased cellular excretion.