Osteopontin deficiency leads to the resolution of prostatic fibrosis and inflammation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA744485 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15058918_1.fastq.gz | Fastqsanger.gz | |||
| SRR15058918_2.fastq.gz | Fastqsanger.gz | |||
| SRR15058919_1.fastq.gz | Fastqsanger.gz | |||
| SRR15058919_2.fastq.gz | Fastqsanger.gz | |||
| SRR15058920_1.fastq.gz | Fastqsanger.gz |
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Project description:The goals of this study is to determine transcriptomic changes in the mouse ventral prostate associated with E. coli-induced chronic inflammation and fibrosis and the alteration of this gene expression signature in osteopontin deficient mice.
2021-11-16 | GSE179655 | GEO
Project description:Fibrogenic and inflammatory processes in the prostate are linked to the development of lower urinary tract symptoms (LUTS) in men. Our previous studies identified that osteopontin (OPN), a pro-fibrotic cytokine, is abundant in the prostate of men with LUTS, and its secretion is stimulated by inflammatory cytokines potentially to drive fibrosis. This study investigates whether the lack of OPN ameliorates inflammation and fibrosis in the mouse prostate. We instilled uropathogenic E. coli (UTI89) or saline (control) transurethrally to C57BL/6J (WT) or Spp1tm1Blh/J (OPN-KO) mice and collected the prostates one or 8 weeks later. We found that OPN mRNA and protein expression were significantly induced by E. coli-instillation in the dorsal prostate (DP) after one week in WT mice. Deficiency in OPN expression led to decreased inflammation and fibrosis and the prevention of urinary dysfunction after 8 weeks. RNAseq analysis identified that E. coli-instilled WT mice expressed increased levels of inflammatory and fibrotic marker RNAs compared to OPN-KO mice including Col3a1, Dpt, Lum and Mmp3 which were confirmed by RNAscope. Our results indicate that OPN is induced by inflammation and prolongs the inflammatory state; genetic blockade of OPN accelerates recovery after inflammation, including a resolution of prostate fibrosis.
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Project description:Osteopontin Deficiency Amerliorates Alport Kindey Pathology
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Project description:Osteopontin tranfected vs empty vector breast cell line Keywords: parallel sample
2004-01-07 | GSE939 | GEO
Project description:Previous studies of tissue repair have revealed osteopontin (OPN) to be up-regulated in association with the wound inflammatory response. We hypothesize that OPN may contribute to inflammation-associated fibrosis. In a series of in vitro and in vivo studies, we analyze the effects of blocking OPN expression at the wound, and determine which inflammatory cells, and which paracrine factors from these cells, may be responsible for triggering OPN expression in wound fibroblasts. Delivery of OPN antisense oligodeoxynucleotides into mouse skin wounds by release from Pluronic gel decreases OPN protein levels at the wound and results in accelerated healing and reduced granulation tissue formation and scarring. To identify which leukocytic lineages may be responsible for OPN expression, we cultured fibroblasts in macrophage-, neutrophil-, or mast cell-conditioned media (CM), and found that macrophage- and mast cell-secreted factors, specifically platelet-derived growth factor (PDGF), induced fibroblast OPN expression. Correspondingly, Gleevec, which blocks PDGF receptor signaling, and PDGF-Rbeta-neutralizing antibodies, inhibited OPN induction by macrophage-CM. These studies indicate that inflammation-triggered expression of OPN both hinders the rate of repair and contributes to wound fibrosis. Thus, OPN and PDGF are potential targets for therapeutic modulation of skin repair to improve healing rate and quality.
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Project description:Memory helper T cells provide long-lasting host defeMemory helper T cells provide long-lasting host defense against microbial pathogens, while distinct subpopulations of memory T cells drive chronic inflammatory diseases such as asthma. Asthma is a chronic allergic inflammatory disease with airway remodeling including fibrotic changes. The immunological mechanisms that induce airway fibrotic changes in allergic inflammation remain unknown. We found that Interleukin-33 (IL-33) enhanced Amphiregulin production by the IL-33 receptor, ST2hi memory T helper-2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling directly reprogramed eosinophils to an inflammatory state with enhanced production of Osteopontin, a key profibrotic immunomodulatory protein. IL-5-producing memory Th2 cells and Amphiregulin-producing memory Th2 cells appeared to cooperate to establish lung fibrosis. The analysis of polyps from patients with eosinophilic chronic rhinosinusitis revealed fibrosis with accumulation of Amphiregulin-producing CRTH2hiCD161hiCD45RO+CD4+ Th2 cells and Osteopontin-producing eosinophils. Thus, the IL-33-Amphiregulin-Osteopontin axis directs fibrotic responses in eosinophilic airway inflammation and is a potential target for the treatment of fibrosis induced by chronic allergic disorders. against microbial pathogens, while distinct subpopulations of memory T cells drive chronic inflammatory diseases such as asthma. Asthma is a chronic allergic inflammatory disease with airway remodeling including fibrotic changes. The immunological mechanisms that induce airway fibrotic changes in allergic inflammation remain unknown. We found that Interleukin-33 (IL-33) enhanced Amphiregulin production by the IL-33 receptor, ST2 hi memory T helper-2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling directly reprogramed eosinophils to an inflammatory state with enhanced production of Osteopontin, a key profibrotic immunomodulatory protein. IL-5-producing memory Th2 cells and Amphiregulin-producing memory Th2 cells appeared to cooperate to establish lung fibrosis. The analysis of polyps from patients with eosinophilic chronic rhinosinusitis revealed fibrosis with accumulation of Amphiregulin-producing CRTH2hiCD161hiCD45RO+CD4+ Th2 cells and Osteopontin-producing eosinophils. Thus, the IL-33-Amphiregulin-Osteopontin axis directs fibrotic responses in eosinophilic airway inflammation and is a potential target for the treatment of fibrosis induced by chronic allergic disorders.
2018-08-21 | GSE114921 | GEO
Project description:Analysis of gene expression in prostatic tissue from BPH patients with and without SRD5A2 gene methylation. The hypothesis is that BPH patients with DNA methylation of the SRD5A2 gene promoter have impaired conversion of testosterone to dihydrotestosterone, and therefore may use an alternative signaling pathway for prostatic tissue growth. Here, we compare gene expression profiles of SRD5A2-methylated vs. unmethylated prostatic tissue to nominate alternative biological pathways relevant in each molecular subtype of BPH.
2017-10-01 | GSE101486 | GEO
Project description:Lower urinary tract symptoms (LUTS) relate to storage and/or voiding disturbances which are common among aging men. Disease etiology is largely unknown, and diagnosis is currently based on subjective symptom scores. While mainstay treatments can be ineffective and bothersome, biomarker discovery efforts may facilitate objective diagnostic criteria for personalized medicine and new potential druggable pathways. Since inflammation is one of its plausible etiologies, the goal of this project is to explore urinary metabolite and protein biomarkers as a non-invasive method to diagnose of LUTS which is induced by inflammation. Herein, a bacterial-induced prostatic inflammation model was established with C57BL/6J mice infected with uropathogenic E. coli 1677. Mouse urine samples were collected from control and treatment mice. Mass Spectrometry-based multi-omics analysis was employed here to discover urinary protein and metabolite-based biomarkers specific to prostatic inflammation-induced LUTS. We investigated the use of isobaric dimethylated leucine (DiLeu) labeling for metabolite identification and quantification for the mouse urine samples, and because of the use of DiLeu labeling, we combined metabolomics and proteomics on the same LC-MS platform. Overall, a total of 143 amine-containing metabolites and 1058 urinary proteins were identified and quantified, among them, 14 metabolites and 168 proteins were significantly changed by the inflammation treatment. Five metabolic pathways and four inflammatory-related biological processes were potentially disrupted. After compare with LUTS patient and other previously report, metabolite creatine and protein Polymeric Ig receptor presents especially attractive combined biomarker for prostatic inflammation induced LUTS and could be further used as the LUTS patient stratification. Overall, this study found urine metabolomics and proteomics to be an informative and noninvasive method for candidate biomarkers determination and etiologies classification of LUTS induced by inflammation.
2021-05-03 | PXD018023 | Pride
Project description:To study role of macrophage derived osteopontin in NASH
2023-03-31 | GSE227328 | GEO
Project description:We define a pathogenic subset of microglia that is distinguished by expression of the CD11c protein and by production of osteopontin (OPN). OPN production by this CD11c+ microglial subset correlates positively with disease pathology and severity in the 5XFAD mouse model and in AD patients. Genetic ablation of OPN in 5XFAD mice leads to reduced development of pro-inflammatory CD11c+ microglia, increased amyloid beta (Aβ) phagocytosis and improved cognitive function.
2023-02-01 | GSE191118 | GEO