Effect of zoledronic acid on FOEC cell gene expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE265990 | GEO | 2025/04/26
REPOSITORIES: GEO
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Project description:Effect of zoledronic acid on FOEC cell gene expression
| PRJNA1105102 | ENA
Project description:Background and Aims: In inflammatory bowel disease, protein misfolding in the endoplasmic reticulum (ER) potentiates epithelial barrier dysfunction and impairs mucosal healing. Tauroursodeoxycholic acid (TUDCA), a naturally occurring bile acid, acts as a chemical chaperone to reduce protein aggregation and colitis severity in preclinical models. We conducted an open label trial evaluating oral TUDCA as therapy in patients with active ulcerative colitis (UC). Methods: Patients with moderate-to-severely active UC (Mayo score ≥6, endoscopic subscore ≥1) received oral TUDCA at 1.75 or 2 g/day for 6 weeks. Exclusion criteria included known hepatic disorders or change in UC therapy within 60 days. Clinical disease activity questionnaires, endoscopy with biopsy, blood, and stool were collected at enrollment and after 6 weeks. The primary outcome measure was change in ER stress markers while safety, tolerability and change in UC disease activity were secondary outcomes. Results: Thirteen participants completed the study with eleven evaluable for clinical response. TUDCA was well-tolerated with transient dyspepsia being the most common side effect. Mucosal biopsies revealed significant reductions in ER stress and inflammation as well as an increase in markers of epithelial restitution. Clinical, endoscopic, and histologic disease activity were significantly improved at week 6 (mean total Mayo Score: 9 to 4.5, p<0.001). Conclusions: Six weeks of oral TUDCA promoted mucosal healing, lessened ER stress, and reduced UC clinical disease activity. TUDCA was safe and well-tolerated in patients with active UC. A randomized controlled trial of adjunctive TUDCA therapy in patients with UC is warranted. ClinicalTrials.gov (NCT04114292).
2025-05-30 | GSE266963 | GEO
Project description:To reveal the molecular mechanisms underlying oral ulcerative mucositis-induced pain, we investigated putative pain-associated mediators, pain-related behaviors and gene modulation in a rat oral mucositis model. On day 1 after acetic acid treatment, the mucosal area showed slight redness and swelling but no evidence of ulceration or pain induction. On day 2, oral ulcers were obvious, as was the induction of spontaneous and mechanical pain. In the treated mucosal area, bacterial loading and prostaglandin E2 increased beginning on day 2; no significant changes were observed on day 1. DNA microarray analysis of trigeminal ganglion tissue collected on day 2 identified 32 significantly regulated genes (>1.5-fold change in expression). The up-regulation of the top 3 genes, Hamp (hepcidin antimicrobial peptide), Reg3b (regenerating islet-derived 3β) and Serpina3n (serine peptidase inhibitor A3N), was validated through quantitative RT-PCR. Systemic antibiotic pre-treatment did not increase the mRNA levels. Therefore, we conclude that the oral ulcerative mucositis-induced pain is caused by infectious inflammation of the ulcerative area and stimulates anti-bacterial and anti-peptidase gene expressions in sensory neurons. Oral ulcerative mucositis-induced gene expression in trigeminal ganglion tissue was measured. Ten Wistar rats were divided into the following two groups, control, oral ulcerative mucositis (stomatitis). Five rats were anesthetized with sodium pentobarbital. A piece of filter paper was soaked in 50% acetic acid diluted with water and placed in the labial fornix region of the inferior incisors of rats for 30 sec. Other five rats received only anesthesia without any treatment were used as a control. On day 2 after acetic acid treatment, oral ulcerative mucositis was obvious and trigeminal ganglion tissues in two groups were collected for DNA microarray analysis.
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Project description:To reveal the molecular mechanisms underlying oral ulcerative mucositis-induced pain, we investigated putative pain-associated mediators, pain-related behaviors and gene modulation in a rat oral mucositis model. On day 1 after acetic acid treatment, the mucosal area showed slight redness and swelling but no evidence of ulceration or pain induction. On day 2, oral ulcers were obvious, as was the induction of spontaneous and mechanical pain. In the treated mucosal area, bacterial loading and prostaglandin E2 increased beginning on day 2; no significant changes were observed on day 1. DNA microarray analysis of trigeminal ganglion tissue collected on day 2 identified 32 significantly regulated genes (>1.5-fold change in expression). The up-regulation of the top 3 genes, Hamp (hepcidin antimicrobial peptide), Reg3b (regenerating islet-derived 3β) and Serpina3n (serine peptidase inhibitor A3N), was validated through quantitative RT-PCR. Systemic antibiotic pre-treatment did not increase the mRNA levels. Therefore, we conclude that the oral ulcerative mucositis-induced pain is caused by infectious inflammation of the ulcerative area and stimulates anti-bacterial and anti-peptidase gene expressions in sensory neurons.
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Project description:While skin and oral mucosa share many morphological similarities, oral mucosal wounds heal more rapidly than skin wounds. Epithelial cells from oral mucosa exhibit increased migratory and proliferative capacities when compared to cells from skin, suggesting that the improved repair of mucosa may involve intrinsic differences in epithelial cells. This is an exploratory experiment to define the differential microRNA expression of baseline unwounded skin and oral mucosa epithelium.
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Project description:Langerhans cells (LCs) populate the mucosal epithelium, a major entry portal for pathogens, yet their ontogeny remains unclear. In contrast to skin LCs originating from self-renewing radioresistant embryonic precursors, we found that oral mucosal LCs derive from circulating radiosensitive precursors. Mucosal LCs can be segregated into CD103+CD11blow (CD103+LCs) and CD11b+CD103- (CD11b+LCs) subsets. We further demonstrated that similar to non-lymphoid dendritic cells (DCs), CD103+LCs originate from pre-DCs, whereas CD11b+LCs differentiate from both pre-DCs and monocytic precursors. Despite this ontogenetic discrepancy between skin and mucosal LCs, transcriptomic signature and immunological function of oral LCs highly resemble those of skin LCs but not DCs. These findings, along with their epithelial position, morphology and expression of LC-associated phenotype strongly suggest that oral mucosal LCs are genuine LCs. Collectively, in a tissue-dependent manner, murine LCs differentiate from at least three distinct precursors (embryonic, pre-DCs and monocytic) in steady state The following cells were isolated from mice (2-4 replicates): Lung DCs, mucosal CD103+ LC, mucosal CD11b+ LC, Skin LC. Transcriptome analysis was performed.
2015-08-31 | E-GEOD-68789 | biostudies-arrayexpress
Project description:In order to identify the processes altered in T regulatory cells (Treg) by Zoledronic acid (ZA), we examined RNA expression by RNA-seq in Treg treated with and without ZA. We identified gene expression alterations in ZA-treated Treg that were essential to Treg function.
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Project description:The oral cavity is a multifunctional organ composed of structurally heterogeneous mucosal tissues that remain poorly characterised. Oral mucosal tissues are highly stratified and segmented along an epithelial–lamina propria axis. Here, we performed spatial transcriptomics (tomo-seq) on the tongue, cheeks, and palate of the adult mouse to understand the cues that maintain the oral mucosal sites. We define unique and shared molecular markers of cellular niches and differentiation programmes across oral sites. Using a comparative approach, we identify fibroblast growth factor (FGF) pathway components as potential niche factors for oral epithelial stem cells. Using organoid technology, we validated three FGF ligands (FGF1, FGF7, FGF10) as regulators of site-specific stemness in the dorsal and ventral tongue epithelium. Our dataset of the spatially resolved genes across major oral sites represents a comprehensive resource for unravelling the molecular mechanisms underlying the adult homeostasis of the oral mucosa and its stem cell niches.
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Project description:In this study, we assess the effect of zoledronic acid on clearance of disseminated tumour cells (DTCs) from the bone marrow in women undergoing neoadjuvant chemotherapy for breast cancer In this dataset, Primary breast tissue from stage II or III breast cancer patients were included in the analysis. This study allowed the identification of novel gene expression patterns associated with the presence of DTCs BM by IHC and supports the concept of epithelial to mesenchymal transition transition (EMT) of DTCs present in the BM .
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