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Objective To evaluate the role of interleukin-4 receptor (IL-4R) in renal fibrosis following renal ischemia-reperfusion (I/R) injury in mice.Methods Twelve male wild type BALB/C mice and 12 IL-4Rα gene-knockout mice,aged 8-10 weeks,weighing 20-30 g,were used in the study.The mice of either type were divided into 2 groups (n =6 each) using a random number table:sham operation group (group S) and group I/R.In group I/R,renal I/R was induced by occlusion of the right renal artery for 1 h with atraumatic microclips followed by 2 weeks of reperfusion.The right renal artery was only isolated in group S.At 2 weeks of reperfusion,blood samples were taken from the orbital vein for determination of the concentrations of serum blood urea nitrogen (BUN) and creatinine (Cr).The renal tissues were obtained,and the renal fibrosis area was measured by Sirius Red staining.The expression of fibronectin (FN),collagen Ⅰ (COL-Ⅰ) and α-smooth muscle actin (α-SMA) in renal tissues was detected by immunofluorescence.The expression of signal transducer and activator of transcription 6 (STAT6) and phospho-STAT6 in renal tissues was determined by Western blot.The ratio of phoshop-STAT6 to STAT6 was calculated to reflect the phosphorylation of STAT6.Results Compared with group S of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly increased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly up-regulated,and the phosphorylation of STAT6 in renal tissues was significantly increased in group I/R of wild type and IL-4Rα KO mice (P＜0.05).Compared with group I/R of wild type mice,the serum BUN and Cr concentrations and renal fibrosis area were significantly decreased,the expression of FN,COL-Ⅰ and α-SMA in renal tissues was significantly down-regulated,and the phosphorylation of STAT6 in renal tissues was significantly decreased in group I/R of IL-4RαKO mice (P＜0.05).Conclusion The mechanism of renal fibrosis following renal I/R injury is partially related to IL-4R,and IL-4R results in renal fibrosis through promoting activation of STAT6 signaling pathway in mice.
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OBJECTIVE To dectect the possible association between interleukin-4 receptor gene polymorphism and allergic rhinitis. METHODS The study was conducted in two different groups: patients with allergic rhinitis (the case group,n=50) and healthy people (the control group,n=40). The IL-4R Q576R polymorphism was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The study compared frequencies distribution of genotype and allele between the two groups,and calculated odds ratio (OR) of genotype. RESULTS IL-4R allelic frequencies showed significant difference between the two groups (x2=9.12,P
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Objective To measure the mRNA expression of interleukin receptors (IL-2R?IL-4R and IL-10R) in peripheral blood mononuclear cells (PBMCs) from patients with chronic idiopathic urticaria (CIU). Methods Thirty CIU patients and 30 controls were enrolled in this study. PBMCs were separated from the peripheral blood specimens. Reverse transcription-polymerase chain reaction (RT-PCR) technique was applied to semi-quantitatively analyze the mRNA expression. Results The expression level of IL-10R mRNA was significantly increased in patients with CIU than that in the healthy controls, while that of IL-2R and IL-4R mRNA in PBMCs showed no significant difference. Conclusion Our results suggest that IL-10R might be involved in the pathogenesis of CIU.
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AIM: To determine whether interleukin 4 and interleukin 4 receptor ? chain are associated with allergic asthma in children and to study the impact of such polymorphism upon plasma IgE.METHODS: Two polymorphism sites of IL-4 and IL-4R were studied by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).RESULTS: (1)The results showed that the IL-4 promoter-589 was not associated with children allergic asthma, however, the IL-4R ? chain 576RR genotype and R allele were significantly increased in the subjects with asthma in children compared with age-matched control subjects (?2=11.84, P