Abstract
BackgroundFra-1 (fosl1) belongs to the activator protein1 (AP-1) family inducing IL-11 expression in oxidative stress condition. IL-11 plays a pivotal role in protecting epithelial barriers integrity. In this study, we investigated the Fra-1 gene expression in the inflamed mucosa of patients with ulcerative colitis (UC) as well as its relation to IL-11 expression.Materials and methodsWe enrolled 20 patients and 20 healthy controls with definite UC based on the clinical criteria. Fra-1 gene expression in inflamed and non-inflamed colonic biopsies was determined by real-time polymerase chain reaction (RT-PCR). The IL-11 protein concentration was measured by Enzyme-Linked Immunosorbent Assay (ELISA) method. Pearson correlation was applied to calculate the relation between Fra-1 and IL-11.ResultsAn increased level of Fra-1 gene expression was observed in patients with mild ulcerative colitis. The protein concentration of IL-11 was also increased in mild UC patients. Conversely, a significant decrease of IL-11 protein level was detected in severe UC patients compared to control group.ConclusionOxidative stress in inflamed intestinal biopsies can induce fra-1 gene expression. Our findings suggest that Fra-1 transcription factor leads to the production of IL-11 protein in UC patients.
Highlights
Fra-1 belongs to the activator protein1 (AP-1) family inducing IL-11 expression in oxidative stress condition
Our findings suggest that Fra-1 transcription factor leads to the production of IL-11 protein in ulcerative colitis (UC) patients
Fra-1 gene expression increased in mild colitis We evaluated the mRNA level of Fra-1 by real-time polymerase chain reaction (RT-PCR) in the inflamed colonic biopsy of mild and severe UC patients
Summary
Fra-1 (fosl1) belongs to the activator protein (AP-1) family inducing IL-11 expression in oxidative stress condition. IL-11 plays a pivotal role in protecting epithelial barriers integrity. We investigated the Fra-1 gene expression in the inflamed mucosa of patients with ulcerative colitis (UC) as well as its relation to IL-11 expression. UC is pathologically diagnosed by inflammation and injury in the gastrointestinal tract. Despite extensive investigations on patients and experimental models, the main causes of UC, in terms of aetiology have not been understood [4]. Recent investigations have reported that oxidative stress plays crucial roles in the pathogenesis of UC [5]. The release of reactive oxygen species (ROS) accompanied by up-regulation of proinflammatory cytokines in intestinal inflammation which leads to activation of various intracellular pathways, such as mitogen-activated
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