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880
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ShareScore release 0.9.0
Dataset results
880 results for “Pathogenesis”
Pro-inflammatory Pathways Contribute to Pathogenesis of Clostridioides difficile Infection in a Murine Model - A Spatial Transcriptomics Study
GEO Series GSE288150. Mus musculus. 187 samples. Type: Other.
Microglial cGAS Deletion Preserves Intercellular Communication and Alleviates Amyloid-β-Induced Pathogenesis of Alzheimer's Disease
GEO Series GSE296510. Mus musculus. 12 samples. Type: Expression profiling by array.
Pseudomonas aeruginosa controls both Caenorhabdtitis elegans attraction and pathogenesis by regulating nitrogen assimilation
GEO Series GSE273751. Pseudomonas aeruginosa. 9 samples. Type: Expression profiling by high throughput sequencing.
Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis
GEO Series GSE242568. Mus musculus. 52 samples. Type: Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing.
Chromosomal abberations and transcriptional characteristics linked to the pathogenesis of diffuse large b-cell lymphomas
GEO Series GSE5138. Homo sapiens. 42 samples. Type: Genome variation profiling by genome tiling array.
Treg cell by tumor-associated macrophage ROS and inflammatory signaling through T-cell NF-κB c-Rel drives pathogenesis of lung adenocarcinomas
GEO Series GSE132460. Homo sapiens. 2 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
An ex vivo human precision-cut lung slice platform provides insight into SARS-CoV-2 pathogenesis and antiviral drug efficacy
GEO Series GSE226702. Homo sapiens. 9 samples. Type: Expression profiling by high throughput sequencing.
Preliminary Evidence for IL-10-Induced ACE2 mRNA Expression in Lung-Derived and Endothelial Cells: Implications for SARS-Cov-2 ARDS Pathogenesis
<p>Angiotensin-converting enzyme 2 (ACE2) is a receptor for the spike protein of SARS-COV-2 that allows viral binding and entry and is expressed on the surface of several pulmonary and non-pulmonary cell types, with induction of a "cytokine storm" upon binding. Other cell types present the receptor and can be infected, including cardiac, renal, intestinal, and endothelial cells. High ACE2 levels protect from inflammation. Despite the relevance of ACE2 levels in COVID-19 pathogenesis, experimental studies to comprehensively address the question of ACE2 regulations are still limited. A relevant observation from the clinic is that, besides the pro-inflammatory cytokines, such as IL-6 and IL-1β, the anti-inflammatory cytokine IL-10 is also elevated in worse prognosis patients. This could represent somehow a "danger signal", an alarmin from the host organism, given the immuno-regulatory properties of the cytokine. Here, we investigated whether IL-10 could increase ACE2 expression in the lung-derived Calu-3 cell line. We provided preliminary evidence of ACE2 mRNA increase in cells of lung origin <em>in vitro</em>, following IL-10 treatment. Endothelial cell infection by SARS-COV-2 is associated with vasculitis, thromboembolism, and disseminated intravascular coagulation. We confirmed ACE2 expression enhancement by IL-10 treatment also on endothelial cells. The sartans (olmesartan and losartan) showed non-statistically significant ACE2 modulation in Calu-3 and endothelial cells, as compared to untreated control cells. We observed that the antidiabetic biguanide metformin, a putative anti-inflammatory agent, also upregulates ACE2 expression in Calu-3 and endothelial cells. We hypothesized that IL-10 could be a danger signal, and its elevation could possibly represent a feedback mechanism fighting inflammation. Although further confirmatory studies are required, inducing IL-10 upregulation could be clinically relevant in COVID-19-associated acute respiratory distress syndrome (ARDS) and vasculitis, by reinforcing ACE2 levels.</p>
Scleroderma-specific autoantibodies embedded in immune complexes mediate endothelial damage: an early event in the pathogenesis of systemic sclerosis
<p><strong>Background: </strong>Consistently with their diagnostic and prognostic value, autoantibodies specific for systemic sclerosis (SSc) embedded in immune complexes (ICs) elicited a pro-inflammatory and pro-fibrotic cascade in healthy skin fibroblasts, engaging Toll-like Receptors (TLRs) via their nucleic acid components. The objective of this study was to investigate the pathogenicity of SSc-ICs in endothelial cells.</p> <p><strong>Methods: </strong>ICs were purified from sera of SSc patients bearing different autoantibody specificities (antibodies against DNA topoisomerase I, centromeric proteins, RNA polymerase and Th/To), patients with systemic lupus erythematosus (SLE), primary anti-phospholipid syndrome (PAPS) or healthy controls (NHS) using polyethylen glycol precipitation. Human umbilical vein endothelial cells (HUVECs) were incubated with ICs, positive and negative controls. mRNA levels of <em>endothelin-1 (et-1)</em>, <em>collagenIα1 (colI</em><em>a</em><em>1)</em>, <em>interferon (IFN)-α</em> and <em>IFN-β</em> were investigated by Real-Time PCR; <em>et-1</em> and <em>il-6</em> mRNA levels were assessed after pre-treatment with bafilomycin. ICAM-1 expression was evaluated by cell-ELISA; secretion of IL-6, IL-8 and transforming growth factor (TGF)-β1 in culture supernatants was measured by ELISA. The expression of Fcg receptors (CD64, CD32 and CD16) was assessed in endothelial cells at FACS analysis. Intracellular signalling pathways culminating with NFkB, p38MAPK, SAPK-JNK and Akt were assessed by Western Blotting. Healthy skin fibroblasts were stimulated with supernatants from HUVEC incubated with ICs, and TGF-b1 secretion, mRNA levels of <em>colIα1</em> and <em>matrix metalloproteinase (mmp)-1</em>, protein expression of a smooth muscle actin (a-SMA) and IL-6 were evaluated by Western Blotting<em>; et-1</em> mRNA levels were assessed in fibroblasts pre-treated with IL-6 and TGF-b inhibitors and stimulated with ATA-ICs.</p> <p><strong>Results: </strong>All SSc stimulated IL-6 secretion; ACA-ICs and anti-Th/To-ICs increased ICAM-1 expression; all SSc-ICs but anti-Th/To-ICs augmented IL-8 levels; all SSc-ICs but ACA and ARA-ICs up-regulated <em>et-1 </em>and all SSc-ICs but ARA-ICs affected TGF-b1 secretion. c<em>olI</em><em>a</em><em>1</em>, <em>IFN-</em><em>a</em> and <em>IFN-</em><em>b </em>mRNA levels were not affected by any SSc-IC. FcgRII (CD32) and FcgRIII (CD16) were not detectable on HUVECs, while FcgRI (CD64) was minimally expressed. A differential modulation of<em> tlr</em> expression was observed: <em>tlr2</em>, <em>tlr3</em> and <em>tlr4</em> were up-regulated by ATA-ICs and ACA-ICs, while anti-Th/To-ICs resulted in <em>tlr9</em> up-regulation. Pre-treatment with bafilomycin did not affect the up-regulation of <em>et-1</em> and <em>il-6</em> induced by ATA-ICs, ACA-ICs and anti-Th/To-ICs; a 23% reduction in both genes was reported for ARA-ICs. All SSc-ICs activated p38MAPK and AKT, all SSc-ICs but ARA-ICs yielded the activation of NFkB; ATA-ICs and ACA-ICs increased the activation rate of both subunits of SAPK-JNK. When healthy skin fibroblasts were stimulated with supernatants from HUVECs incubated with SSc-ICs, TGF-b1 secretion, <em>colI</em><em>a</em><em>1, </em>a-SMA and IL-6 expression levels were significantly modulated. Pre-treatment with IL-6 and TGF-b inhibitors prevented <em>et-1</em> up-regulation induced by ATA-ICs by 85% and 77% respectively.</p> <p><strong>Conclusions: </strong>These data provide the first demonstration of the pathogenicity of ICs from scleroderma patients with different autoantibodies on the endothelium. Endothelial activation induced by SSc-ICs ultimately led to a pro-fibrotic phenotype in healthy skin fibroblasts.</p>
Arthritis pathogenesis: Development of novel diagnostic and therapeutic approaches
GEO Series GSE27358. Homo sapiens; Mus musculus. 4 samples. Type: Expression profiling by array.
Identification of molecular mechanisms involved in pathogenesis of MALT lymphoma from small sample size
GEO Series GSE16024. Homo sapiens. 62 samples. Type: Expression profiling by array.
Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (tRF overexpression)
GEO Series GSE242561. Mus musculus. 16 samples. Type: Expression profiling by high throughput sequencing.
A tumor suppression role for EZH2 in Diffuse Intrinsic Pontine Glioma pathogenesis
GEO Series GSE188450. Mus musculus. 14 samples. Type: Expression profiling by high throughput sequencing.
Several key elements in the pathogenesis of severe udder cleft dermatitis as revealed by RNA transcriptomics
GEO Series GSE221364. Bos taurus. 15 samples. Type: Expression profiling by high throughput sequencing.
Role of the prophages in the Staphylococcus aureus pathogenesis
GEO Series GSE26623. Staphylococcus aureus. 36 samples. Type: Expression profiling by array.
Role of tRNA-derived fragments in the cross-talk between immune cells and beta cells during type 1 diabetes pathogenesis (PD in vivo)
GEO Series GSE242563. Mus musculus. 10 samples. Type: Non-coding RNA profiling by high throughput sequencing.
YTHDF1-CLOCK axis contributes to pathogenesis of allergic airway inflammation through LLPS [mRNA-seq]
GEO Series GSE256531. Mus musculus. 4 samples. Type: Expression profiling by high throughput sequencing.
Inhibition of TET1 prevents the development of Osteoarthritis and reveals the 5hmC landscape that orchestrates pathogenesis
GEO Series GSE143576. Mus musculus. 36 samples. Type: Expression profiling by high throughput sequencing; Methylation profiling by high throughput sequencing.
Targets of Bmi1 in HCC pathogenesis
GEO Series GSE97172. Mus musculus; Homo sapiens. 10 samples. Type: Expression profiling by array.
ZNF598 co-translationally titrates poly(GR) protein implicated in the pathogenesis of C9ORF72-associated ALS/FTD
<p><em>C9ORF72</em>-derived dipeptide repeat proteins have emerged as the pathogenic cause of neurodegeneration in amyotrophic lateral sclerosis and frontotemporal dementia (C9-ALS/FTD). However, the mechanisms underlying their expression are not fully understood. Here, we demonstrate that ZNF598, the rate-limiting factor for ribosome-associated quality control (RQC), co-translationally titrates the expression of <em>C9ORF72</em>-derived poly(GR) protein. A <em>Drosophila</em> genetic screen identified key RQC factors as potent modifiers of poly(GR)-induced neurodegeneration. ZNF598 overexpression in human neuroblastoma cells inhibited the nuclear accumulation of poly(GR) protein and decreased its cytotoxicity, whereas <em>ZNF598</em> deletion had opposing effects. Poly(GR)-encoding sequences in the reporter RNAs caused translational stalling and generated ribosome-associated translation products, sharing molecular signatures with canonical RQC substrates. Furthermore, ZNF598 and listerin 1, the RQC E3 ubiquitin-protein ligase, promoted poly(GR) degradation via the ubiquitin-proteasome pathway. An ALS-relevant ZNF598<sup>R69C</sup> mutant displayed loss-of-function effects on poly(GR) expression, as well as on general RQC. Moreover, RQC function was impaired in C9-ALS patient-derived neurons, whereas lentiviral overexpression of ZNF598 lowered their poly(GR) expression and suppressed proapoptotic caspase-3 activation. Taken together, we propose that an adaptive nature of the RQC-relevant ZNF598 activity allows the co-translational surveillance to cope with the atypical expression of pathogenic poly(GR) protein, thereby acquiring a neuroprotective function in C9-ALS/FTD.</p>
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.