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Disease associated fibroblasts from various pancreatic disorders exhibit subtype specific genetic profile [miRNA]

ABSTRACT: Currently it is unknown whether activation of recruited or resident pancreatic fibroblasts, including pancreatic stellate cells activation, create a common “fibroblast-activated phenotype” indistinguishable from their associated-diseased microenvironment . Using a combination of microRNA and mRNA profiling of fibroblasts isolated from pancreatic ductal adenocarcinoma (PDAC), chronic pancreatitis (CP), periampullary cancer (PAT) and areas of histologically normal pancreas, followed by comprehensive validation, we show that activated fibroblasts derived from different pancreatic disease types are considerably distinct.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE123377 | GEO | 2020/07/14

REPOSITORIES: GEO

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Disease associated fibroblasts from various pancreatic disorders exhibit subtype specific genetic profile [RNA]

Project description:Currently it is unknown whether activation of recruited or resident pancreatic fibroblasts, including pancreatic stellate cells activation, create a common “fibroblast-activated phenotype” indistinguishable from their associated-diseased microenvironment . Using a combination of microRNA and mRNA profiling of fibroblasts isolated from pancreatic ductal adenocarcinoma (PDAC), chronic pancreatitis (CP), periampullary cancer (PAT) and areas of histologically normal pancreas, followed by comprehensive validation, we show that activated fibroblasts derived from different pancreatic disease types are considerably distinct.

2020-07-14 | GSE123375 | GEO

NADPH Oxidase 1 in Chronic Pancreatitis-Activated Pancreatic Stellate Cells Facilitates the Progression of Pancreatic Cancer

Project description:Aims: Patients suffering from chronic pancreatitis (CP) have a higher risk of pancreatic ductal adenocarcinoma (PDAC). NADPH oxidase 1 (Nox1) in activated pancreatic stellate cells from a CP mouse model (CP-activated PaSCs) forms fibrotic tissue and up-regulates matrix metalloproteinase (MMP) 9. Yet, the role and mechanism of Nox1 in CP-activated PaSCs in the progression of PDAC is unknown. 1) We tested the ability of Nox1 in CP-activated PaSCs to facilitate the growth and invasion of pancreatic cancer cells. 2) We identified proteins in the secretome of CP-activated PaSCs whose production was Nox1-dependent. Results: In vitro, Nox1 in CP-activated PaSCs facilitated the migration/invasion of MIA PaCa-2 and HPAC cells. Nox1 evoked a both pro-invasive and cancer-promoting phenotype in PaSCs via a paracrine activation of both p38 MAPK and STAT3 pathways in neoplastic cells. In vivo, Nox1 in CP-activated PaSCs facilitated tumor growth, metastasis formation, and stromal expansion. Using mass spectrometry, we identified proteins protecting from cellular stresses in the secretome of CP-activated PaSCs whose production was Nox1-dependent. Innovation: Inhibiting the stromal Nox1 signaling at early stages can reduce the reorganization of histological barriers, and the protection of neoplastic cells from cellular stresses, ameliorating the progression of PDAC. Conclusions: Nox1 in CP-activated PaSCs induced both Twist1 and MMP-9 expression, causing changes in the extracellular matrix composition. In addition, Nox1 oxidized peroxiredoxins 1 and 4 through thioredoxin reductase 1, causing p38 MAPK and STAT3 phosphorylation in neoplastic cells when they were secreted from CP-activated PaSCs. Both mechanisms facilitated the progression of PDAC.

2023-03-10 | PXD034177 | Pride

Single-cell transcriptomic analysis of mouse pancreas: characteristic features of pancreatic ductal cells in chronic pancreatitis

Project description:Chronic pancreatitis (CP) is a pathogenically complex fibro-inflammatory disorder of the pancreas. Our understanding of CP pathogenesis is partly limited by the incomplete characterization of pancreatic cell types. Here, we performed single-cell RNA sequencing on 3,386 cells from the pancreas of one control mouse and mice with caerulein-induced CP. These data provides a preliminary description of the single-cell transcriptome profiles of mouse pancreata and accurately demonstrates the characteristics of pancreatic ductal cells in CP.

2022-06-30 | GSE204844 | GEO

Global microRNA expression profiling of microdissected tissues from diseased and non-diseased pancreatic tissues

Project description:Global microRNA expression profiling of microdissected pancreatic tissues were collected using Agilent miRNA microarrays (G4470B, Sanger 10.1) carrying 723 individual human miRNA probes. Four different sources of RNA were analyzed: microdissected normal pancreatic ductal cells (ND, n=4),microdissected acinar cells (AC, n=4), macrodissected chronic pancreatitis (CP, n=5) and micordissected xenograft tissues derived from primary pancreatic ductal adenocarcinomas (PDAC, n=5). Four condition (AZ, ND, PDAC, CP), each condition is represented by 4 to 5 biological replicates

2011-09-28 | E-GEOD-25820 | biostudies-arrayexpress

Microarray gene-expression data to validate a 17-gene biomarker obtained from excessive meta-analysis to test its PDAC specificity in the presence of pancreatitis tissues.

Project description:Clinical signs and radiographic findings of PDAC and pancreatitis are often indistinguishable, highlighting the need of a PDAC biomarker to be insensitive to pancreatitis. Therefore we validated a biomarker signature of 17-genes in this gene expression data containing PDAC, non-tumor pancreatic and pancreatitis of fresh-frozen and formalin-fixed paraffin-embedded tissues.

2018-05-11 | GSE101462 | GEO

Non-canonical Hedgehog signaling via GLI2 promotes pancreatic stellate cell activation and fibrosis in chronic pancreatitis

Project description:Excessive Hedgehog (Hh) signaling activity contributes to fibrosis in multiple organs, however, its role in pancreatic stellate cell (PSC) activation and fibrosis development during chronic pancreatitis (CP) remains unclear. We demonstrate that GLI2 is upregulated in activated PSCs from CP patients and animal models. Specific deletion of Gli2, but not Smo, significantly alleviated fibrosis in CP models, indicating that CP is driven by non-canonical Hh signaling. Experiments on culture-activated primary PSCs reveal early nuclear translocation and increased GLI2 expression promptly after in vitro culture, with GLI2 being essential for PSC activation. SMO inhibition only reduces GLI2 activation in the short term, while activation of GLI2 by TGF-β/SMAD3 signaling explains the SMO-independent mechanisms leading to Hh activation in PSCs. Altogether, our data demonstrate the activation of the non-canonical Hh pathway in PSCs and indicate that GLI2 represents a promising therapeutic target for CP.

2024-11-13 | GSE281427 | GEO

Potential regulatory proteins in pancreatitis were screened by proteomics using pancreatic tissues of PRSS1 AP mice

Project description:Humanized PRSS1 transgenic mice were constructed and treated with caerulein to mimic the development of human AP and CP. Potential regulatory proteins in pancreatitis were screened by proteomics using pancreatic tissues of PRSS1 AP mice.

2021-09-09 | PXD016651 | Pride

Potential ATF6 regulatory proteins were screened by proteomics using pancreatic tissues of PRSS1 transgenic mice treated with caerulein

Project description:Humanized PRSS1 transgenic mice were constructed and treated with caerulein to mimic the development of human AP and CP. Potential ATF6 regulatory proteins in pancreatitis were screened by proteomics using pancreatic tissues of PRSS1 AP mice.

2021-09-09 | PXD016703 | Pride

Chronic pancreatitis vs pancreatic cancer LC-MS

Project description:Age-standardized incidence rates for pancreatic cancer (PC) in men have increased by 25% from 1957 to 2011 in Finland. The average age of diagnosis for PC is 69 years in Nordic males, whereas the average age of diagnosis of chronic pancreatitis (CP) is 40-50 years, but the cases overlap in age. By radiology the evaluation of a pancreatic mass, i.e. the differential diagnosis between CP and PC is often difficult. Preoperative needle biopsies are difficult to obtain and are demanding to interpret. New blood based biomarkers are needed. The accuracy of the only established biomarker for PC, CA 19-9 is rather poor in differentiating between benign and malignant mass of the pancreas. In this study, we have performed mass spectrometry HDMSE analysis of serum samples from patients with chronic pancreatitis and pancreatic cancer. We have quantified 652 proteins and performed detailed statistical analysis such as principal component analysis, orthogonal partial least square discriminant analysis and receiver operating curve analysis.

2017-06-09 | PXD005144 | Pride

Profiling of Kallikrein Proteases and Global Proteome Biology of PDAC, Chronic Pancreatitis and Normal Pancreas

Project description:Cell conditioned medium from human pancreatic cancer cell lines MiaPaCa-2, AsPC-1, primary pancreatic cell lines as well as human FFPE tissue samples from pancreatic ductal adenocarcinoma (PDAC), chronic pancreatitis (CP), ampullary cancer, non-malignant adjacent pancreas and normal pancreas were analyzed via targeted (SRM, PRM) and/or explorative (DIA) mass spectrometry.

| MSV000090255 | MassIVE

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