Project description:The purpose of this study was to identify long noncoding RNAs (lncRNAs) that are dysregulated during vascular inflammation and contribute to mRNA regulation. Previous studies have suggested that many lncRNAs interact with protein complexes to regulate their neighboring mRNAs. Therefore, we performed the Human LncRNA Expression Microarray V3.0 (Arraystar) to simultaneously profile the expression of lncRNAs and mRNAs under basal conditions and upon stimulation with IL-1β in human umbilical vein endothelial cells (HUVECs). Following, we identified neighboring IL-1β mRNA-lncRNA pairs and found them to be highly correlation in expression. This observation was particularly true when the pairs were found within the same chromatin neighborhood. We also observed mRNA-lncRNA pairs to be mainly divergent transcribed and share common regulatory elements.
Project description:The conditioned media from Bifidobacterium infantis (BCM) and Lactobacillus acidophilus (LCM) were reported to promote maturation of innate immune response gene expression, which explained the protective effects of probiotics in clinical necrotizing enterocolitis. We used microarray analysis to investigate the expression of genes involved in regulation of BCM and LCM in IL-1β stimulated immature human enterocytes. The H4 cells (a human nontransformed primary intestinal epithelial cell line) were pretreated with BCM or LCM (15%) for 30 minutes, and then stimulated with or without IL-1β (10 ng/mL) for 4 h. Cell media and IL-1β stimulation were negative and positive control, respectively. RNA was extracted for mcroarray analysis. A total of six treatments (triplicates for each) were included in this study. As one RNA sample in IL-1β-stimulated cells treated with BCM was dropped due to bad quality, seventeen samples were analyzed. Various treatments were compared to the nagative control (cell media alone). Genes with a fold-change ≥2 and a p value ≤ 0.05 were selected.
Project description:The conditioned media from Bifidobacterium infantis (BCM) and Lactobacillus acidophilus (LCM) were reported to promote maturation of innate immune response gene expression, which explained the protective effects of probiotics in clinical necrotizing enterocolitis. We used microarray analysis to investigate the expression of genes involved in regulation of BCM and LCM in IL-1β stimulated immature human enterocytes. The H4 cells (a human nontransformed primary intestinal epithelial cell line) were pretreated with BCM or LCM (15%) for 30 minutes, and then stimulated with or without IL-1β (10 ng/mL) for 4 h. Cell media and IL-1β stimulation were negative and positive control, respectively. RNA was extracted for mcroarray analysis.
Project description:In the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-α) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors. In order to identify potentially new soluble factors which greatly impact the self-renewal, proliferation and differentiation of CD34+ hematopoietic stem cells (HSC), we examined the expression profiles of IL-1ß, IL-3 and IL-6 stimulated human umbilical vein endothelial cells (HUVEC).
Project description:The objective was to study the time-course effects of interleukin-1β (IL-1β) on equine articular cartilage, with the aim to identify genes of relevance for cartilage pathology in osteoarthritis. Changes in gene expression related to inflammation, extracellular matrix, and phenotypic alterations was studied.
Project description:Toll-like receptors/Interleukin-1 receptor (IL-1R) signaling plays an important role in High-fat diet (HFD)-induced adipose tissue dysfunction contributing to obesity-associated metabolic syndromes. Here, we show an unconventional IL-1R-IRAKM (IL-1R-associated kinase M)-Slc25a1 signaling axis in adipocytes that reprograms lipogenesis to promote diet-induced obesity. Adipocyte-specific deficiency of IRAKM reduced HFD-induced body weight gain, increased whole body energy expenditure and improved insulin resistance, associated with decreased lipid accumulation and adipocyte cell sizes. IL-1β stimulation induced the translocation of IRAKM Myddosome to mitochondria to promote de novo lipogenesis in adipocytes. Mechanistically, IRAKM interacts with and phosphorylates mitochondrial citrate carrier Slc25a1 to promote IL-1β-induced mitochondrial citrate transport to cytosol and de novo lipogenesis. Moreover, IRAKM-Slc25a1 axis mediates IL-1β induced Pgc1a acetylation to regulate thermogenic gene expression in adipocytes. IRAKM kinase-inactivation also attenuated HFD-induced obesity. Taken together, our study suggests that the IL-1R-IRAKM-Slc25a1 signaling axis tightly links inflammation and adipocyte metabolism, indicating a novel therapeutic target for obesity.
Project description:HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of primary fibroblasts from HOIL-1-, MYD88- and NEMO-deficient patients. Primary fibroblasts were obtained from HOIL-1, MYD88- and NEMO-deficient patients and healthy donors and stimulated with TNF-α or IL-1β for 2 and 6 hours. RNA were extracted and globin reduced. Labeled cRNA were hybridized to Illumina Human HT-12 Beadchips.
Project description:In the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-α) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors. In order to identify potentially new soluble factors which greatly impact the self-renewal, proliferation and differentiation of CD34+ hematopoietic stem cells (HSC), we examined the expression profiles of IL-1ß, IL-3 and IL-6 stimulated human umbilical vein endothelial cells (HUVEC). we processed seven different umbilical cords and isolated 129 samples for total RNA, and pooled them into 18 groups corresponding to each stimulant, control and time point.
Project description:To understand the transcripts regulated by inflammation and how this regulation may differ between different individuals, the transcriptome of HUVECs stimulated with inflammatory mediators was examined in 9 different individuals. In the study present here, HUVEC isolates from 9 different individuals were cultured until passage 4 in fully supplemented growth conditions. Passage 4 HUVEC isolates were then treated with a cocktail of inflammatory mediators (10ng/ml TNF-α, Il-1β, Il-8) for a period of 24 hours prior to RNA extraction. RNA was extracted and hybridised onto CodeLink microarrays. The expression profiles in the inflammatory mediator treated condition were examined along side a superset of the same biological replicates that were untreated (also submitted), to facilitate assessment of the resting transcriptome.