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Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

ABSTRACT: Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

ORGANISM(S): Mus musculus

PROVIDER: GSE241626 | GEO | 2023/08/28

REPOSITORIES: GEO

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Similar Datasets

Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

Project description:Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

| PRJNA1009007 | ENA

4-octyl itaconate attenuate experimental acute pancreatitis via inhibiting Sting signaling pathway and activating Nrf2 pathway in macrophages

Project description:Acute pancreatitis (AP) is a common and severe inflammatory disease of the abdomen. Recent studies have shown that macrophages play a crucial role in AP. 4-octyl itaconate (4OI), a derivative of the cell metabolism intermediate itaconate (ITA), has demonstrated significant anti-inflammatory effects in various cell and disease models. In this study, we investigated the potential role and mechanism of 4OI in both in vivo and in vitro models of AP.After administering 25 mg/kg of 4OI to mice and inducing AP with caerulein or L-Arg, we found that 4OI significantly alleviated the severity of AP: serum amylase and lipase levels were significantly reduced, histopathological scores decreased, and levels of inflammatory factors were notably lower. Additionally, macrophage infiltration and M1 polarization were significantly reduced. Through in vitro experiments, we further explored the molecular mechanism by which 4OI inhibits the inflammatory response in macrophages. We discovered that 4OI reduces macrophage polarization to the pro-inflammatory M1 type and decreases the expression of inflammation-related genes. We also found that 4OI exerts its anti-inflammatory effects by promoting the Nrf2 signaling pathway and inhibiting the Sting signaling pathway. In conclusion, this study reveals the anti-inflammatory effects of 4OI in AP and its potential clinical therapeutic value.

2024-09-18 | GSE277097 | GEO

Gene expression in lung tissue, blood and spleen of mice with severe acute pancreatitis

Project description:Severe acute pancreatitis (SAP) is a critical disease, often complicated with multiple organ dysfunction, which seriously endangeres the life safety of patients. Previous studies have shown that cGAS-STING signaling pathway is significantly activated in mice with severe acute pancreatitis. In this study, we studied the gene expression in different tissues of normal mice and SAP mice to understand the differentially expressed genes and find the downstream genes of cGAS-STING signaling pathway.

2023-11-01 | GSE244335 | GEO

4-octyl itaconate attenuate experimental acute pancreatitis via inhibiting Sting signaling pathway and activating Nrf2 pathway in macrophages

Project description:4-octyl itaconate attenuate experimental acute pancreatitis via inhibiting Sting signaling pathway and activating Nrf2 pathway in macrophages

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Transcription profiling of human pancreas from patients with autoimmune pancreatitis and alcohol-induced chronic pancreatitis

Project description:Autoimmune pancreatitis (AIP) is a recently identified disease of the pancreas with unknown etiology and antigens. The aim of this study was to determine new target antigens and differentially regulated genes and proteins by means of transcriptomics and proteomics and to validate them in patients with autoimmune pancreatitis. Here we report a distinct downregulation at the RNA and protein level of pancreatic proteases (anionic trypsinogen, cationic trypsinogen, mesotrypsinogen, elastase IIIB) and pancreatic stone protein in autoimmune pancreatitis in comparison to alcohol-induced chronic pancreatitis.

2008-12-31 | E-MEXP-804 | biostudies-arrayexpress

RNA-Seq of isolated pancreatic stellate cells from mice with autoimmune pancreatitis and chronic pancreatitis

Project description:Autoimmune pancreatitis (AIP) is a disease with unclear immunologic triggers. This study shows that the pancreatic stellate cells(PSCs) are involved in the regulation of the immune response and can cause autoimmunity when the NF-κB signalling in these cells is disrupted. The PSCs were isolated from animals which show autoimmune pancreatitis (NEMO knockout group) or chronic pancreatitis (NEMO wildtype group).

2023-06-30 | E-MTAB-7337 | biostudies-arrayexpress

mRNA expression pattern of KrasG12D mice with acute pancreatitis compared with wild-type mice without acute pancreatitis

Project description:Transgenic KrasG12D mice can recapitulate pancreas intra-epithelial neoplasia (PanIN). Caerulein is a cholecystokinin analogue and induces acute pancreatitis when injected intra-abdominally. Caerulein-induced acute pancreatitis will accelerate PanIN progression in KrasG12D mice. We compared mRNA profile changes between KrasG12D mice with acute caerulein-induced pancreatitis and wild-type mice without acute pancreatitis. The experiment had two groups. Experiment group: KrasG12D mice with acute caerulein-induced pancreatitis (N=6). Three mice in experiment group received 1-week caerulein injection, and the other three mice received 2-week caerulein injection. All experiment group mice started to receive caerulein injection at 1-month of age, and were sacrificed at the last day of caerulein injection. Control group: wild-type mice without acute pancreatitis (N=6). The mice were sacrificed at 1.5-month of age. Whole pancreas tissue lysate samples were subjected to mRNA array assay.

2016-05-14 | E-GEOD-77983 | biostudies-arrayexpress

Inflammation-Driven Carcinogenesis is Mediated through STING [MEFs]

Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from wild type murine embryonic fibroblasts (WT MEFs), STING deficient MEFs (SKO), Trex1 deficient MEFs (TKO), and both STING and Trex1 deficient MEFs (STKO) treated with DMBA and examined cytokine production by these cells.

2014-05-31 | E-GEOD-57603 | biostudies-arrayexpress

Tectochrysin alleviates Ang II-induced pathological cardiac hypertrophy by binding to STING and inhibiting STING/NFκB-mediated inflammation

Project description:Angiotensin II (Ang II)-induced cardiac inflammation plays a pivotal role in the pathogenesis of pathological cardiac hypertrophy and hypertension-related heart failure. Tectochrysin (Tec) is a flavonoid natural compound exhibiting significant anti-inflammatory activity. However, the role of Tec in hypertensive heart failure and its molecular targets remain unclear. The therapeutic efficacy of Tec was assessed in the Ang II-induced mouse model using echocardiography, histopathological staining, and serological tests. Its anti-hypertrophic effect was further examined in vitro by phalloidin staining. Investigate the mechanism of action of Tec through transcriptome sequencing. The interaction of Tec with STING was detected by DARTS, CETSA, and SPR assays. Western blotting assay detected the effect of Tec on Ang II-induced activation of the STING/NFκB pathway. The functional dependency of Tec on STING was demonstrated using the STING inhibitor H151. In vivo experiments confirmed that Tec alleviates Ang II-induced myocardial inflammation, pathological hypertrophy, myocardial fibrosis, and cardiac dysfunction. Further in vitro studies revealed the efficacy of Tec in inhibiting cardiomyocyte hypertrophy. Mechanistically, Tec significantly suppressed Ang II-induced activation of the STING/NFκB signalling pathway by targeting STING. Crucially, administration of the STING inhibitor H151 alleviates pathological myocardial hypertrophy, however its use diminishes the therapeutic effect of Tec. Our findings confirmed STING as a critical therapeutic target in pathological ventricular remodeling, with Tec exerting its anti-hypertrophic effects through STING inhibition.

2026-04-20 | GSE327509 | GEO

Inflammation-Driven Carcinogenesis is Mediated through STING [skin]

Project description:Chronic stimulation of innate immune pathways by microbial agents or damaged tissue is known to promote inflammation-driven tumorigenesis by unclarified mechanisms1-3. Here we demonstrate that mutagenic 7,12-dimethylbenz(a)anthracene (DMBA), etoposide or cisplatin induces nuclear DNA leakage into the cytosol to intrinsically activate STING (Stimulator of Interferon Genes) dependent cytokine production. Inflammatory cytokine levels were subsequently augmented in a STING-dependent extrinsic manner by infiltrating phagocytes purging dying cells. Consequently, STING-/- mice, or wild type mice adoptively transferred with STING-/- bone marrow, were almost completely resistant to DMBA-induced skin carcinogenesis compared to their wild type counterparts. Our data emphasizes, for the first time, a role for STING in the induction of cancer, sheds significant insight into the causes of inflammation-driven carcinogenesis, and may provide therapeutic strategies to help prevent malignant disease Total RNA obtained from DMBA or acetone treated wild type (WT) or STING deficient (SKO) mouse skin or skin tumor was examined for gene expression.

2014-05-31 | E-GEOD-57604 | biostudies-arrayexpress

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