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22
datasets available to search
ShareScore release 0.9.0
Dataset results
22 results for “PTX3”
Evaluation of DiaSorin LIAISON® PTX3 (Long Pentraxin 3) Assay in Patients With Pneumonia
ClinicalTrials.gov study NCT06491004. IPD Sharing: NO. Countries: 1. Publications: 1.
The Effect of Renin Angiotensin System Blockage (RAS) Blockade On PTX3 Levels In Diabetic Patients With Proteinuria
ClinicalTrials.gov study NCT00674596. IPD Sharing: Not stated. Countries: 1. Publications: 1.
The Effects of Renin Angiotensin System Blockage (RAS), Calcium Channel Blocker and Combined Drugs on TWEAK, PTX3 and FMD Levels in Diabetic Proteinuric Patients With Hypertension
ClinicalTrials.gov study NCT00921570. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Macrophage expression and prognostic significance of the long pentraxin PTX3 in COVID-19
GEO Series GSE160351. Homo sapiens. 9 samples. Type: Expression profiling by high throughput sequencing.
POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [HMLER_sublines]
GEO Series GSE130575. Homo sapiens. 7 samples. Type: Expression profiling by high throughput sequencing.
Association of Plasma PTX3 Concentration and Outcomes of STEMI
ClinicalTrials.gov study NCT03894176. IPD Sharing: NO. Countries: 1. Publications: 0.
Effect of LDL-apheresis on PTX3 Plasma Levels in Hypercholesterolemic Patients
ClinicalTrials.gov study NCT01678521. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Clusterin, Ptx3 and Pediatric Febrile Neutropenia (CluPPFeN)
ClinicalTrials.gov study NCT05584930. IPD Sharing: Not stated. Countries: 1. Publications: 0.
PTX3-targeted Antifungal Prophylaxis
ClinicalTrials.gov study NCT03828773. IPD Sharing: Not stated. Countries: 3. Publications: 0.
PTX3 secreted by human adipose-derived stem cells promotes dopaminergic neuron repair in Parkinson's disease via inhibiting apoptosis.
GEO Series GSE163176. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Gene expression profiling of TNBC cells engineered to knock-down or overexpress PTX3
GEO Series GSE188315. Homo sapiens. 12 samples. Type: Expression profiling by array.
RNA-seq analysis revealed that the cardiotoxicity caused by herceptin is due to the release of PTX3.
GEO Series GSE200325. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [MCF10AT_POSH2_OE]
GEO Series GSE130576. Homo sapiens. 2 samples. Type: Expression profiling by high throughput sequencing.
POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation
GEO Series GSE130577. Homo sapiens. 11 samples. Type: Expression profiling by high throughput sequencing.
POSH2 Promotes Breast Cancer Stem-Like Properties through JNK Activation and PTX3 Upregulation [PTX3_OE]
GEO Series GSE130572. Homo sapiens. 2 samples. Type: Expression profiling by high throughput sequencing.
Differenatiation of mRNA expression in PTX3-depleted macrophages
GEO Series GSE192726. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Dataset related to article "Circulating and synovial Pentraxin-3 (PTX3) expression levels correlate with rheumatoid arthritis severity and tissue infiltration indepndently of comventional treatements response."
<p>This record contains raw data related to article “Circulating and synovial Pentraxin-3 (PTX3) expression levels correlate with rheumatoid arthritis severity and tissue infiltration indepndently of comventional treatements response."</p> <p><strong>Aims: </strong>To determine the relationship between PTX3 systemic and synovial levels and the clinical features of rheumatoid arthritis (RA) in a cohort of early, treatment naïve patients and to explore the relevance of PTX3 expression in predicting response to conventional-synthetic (cs) Disease-Modifying-Anti-Rheumatic-Drugs (DMARDs) treatment.</p> <p><strong>Methods: </strong>PTX3 expression was analyzed in 119 baseline serum samples from early naïve RA patients, 95 paired samples obtained 6-months following the initiation of cs-DMARDs treatment and 43 healthy donors. RNA-sequencing analysis and immunohistochemistry for PTX3 were performed on a subpopulation of 79 and 58 synovial samples, respectively, to assess PTX3 gene and protein expression. Immunofluorescence staining was performed to characterize PTX3 expressing cells within the synovium.</p> <p><strong>Results: </strong>Circulating levels of PTX3 were significantly higher in early RA compared to healthy donors and correlated with disease activity at baseline and with the degree of structural damages at 12-months. Six-months after commencing cs-DMARDs, a high level of PTX3, proportional to the baseline value, was still detectable in the serum of patients, regardless of their response status. RNA-seq analysis confirmed that synovial transcript levels of PTX3 correlated with disease activity and the presence of mediators of inflammation, tissue remodeling and bone destruction at baseline. PTX3 expression in the synovium was strongly linked to the degree of immune cell infiltration, the presence of ectopic lymphoid structures and seropositivity for autoantibodies. Accordingly, PTX3 was found to be expressed by numerous synovial cell types such as plasma cells, fibroblasts, vascular and lymphatic endothelial cells, macrophages, and neutrophils. The percentage of PTX3-positive synovial cells, although significantly reduced at 6-months post-treatment as a result of global decreased cellularity, was similar in cs-DMARDs responders and non-responders.</p> <p><strong>Conclusion: </strong>This study demonstrates that, early in the disease and prior to treatment modification, the level of circulating PTX3 is a reliable marker of RA activity and predicts a high degree of structural damages at 12-months. In the joint, PTX3 associates with immune cell infiltration and the presence of ectopic lymphoid structures. High synovial and peripheral blood levels of PTX3 are associated with chronic inflammation characteristic of RA. Additional studies to determine the mechanistic link are required.</p>
The Predictive Role of Preoperative Pentraxin-3 (PTX3) in Metabolic and Inflammatory Outcomes After Roux-en-Y Gastric Bypass
ClinicalTrials.gov study NCT07241741. IPD Sharing: NO. Countries: 0. Publications: 0.
Effect of PTX3 on gene expression of THP-1 macrophages
GEO Series GSE227402. Homo sapiens. 2 samples. Type: Expression profiling by high throughput sequencing.
Dataset related to article " PTX3 Regulation of Inflammation, Hemostatic Response, Tissue Repair, and Resolution of Fibrosis Favors a Role in Limiting Idiopathic Pulmonary Fibrosis."
<p>This record contains data related to article "PTX3 Regulation of Inflammation, Hemostatic Response, Tissue Repair, and Resolution of Fibrosis Favors a Role in Limiting Idiopathic Pulmonary Fibrosis."</p> <p>PTX3 is a soluble pattern recognition molecule (PRM) belonging to the humoral innate immune system, rapidly produced at inflammatory sites by phagocytes and stromal cells in response to infection or tissue injury. PTX3 interacts with microbial moieties and selected pathogens, with molecules of the complement and hemostatic systems, and with extracellular matrix (ECM) components. In wound sites, PTX3 interacts with fibrin and plasminogen and favors a timely removal of fibrin-rich ECM for an efficient tissue repair. Idiopathic Pulmonary Fibrosis (IPF) is a chronic and progressive interstitial lung disease of unknown origin, associated with excessive ECM deposition affecting tissue architecture, with irreversible loss of lung function and impact on the patient's life quality. Maccarinelli et al. recently demonstrated a protective role of PTX3 using the bleomycin (BLM)-induced experimental model of lung fibrosis, in line with the reported role of PTX3 in tissue repair. However, the mechanisms and therapeutic potential of PTX3 in IPF remained to be investigated. Herein, we provide new insights on the possible role of PTX3 in the development of IPF and BLM-induced lung fibrosis. In mice, PTX3-deficiency was associated with worsening of the disease and with impaired fibrin removal and subsequently increased collagen deposition. In IPF patients, microarray data indicated a down-regulation of PTX3 expression, thus suggesting a potential rational underlying the development of disease. Therefore, we provide new insights for considering PTX3 as a possible target molecule underlying therapeutic intervention in IPF.</p>
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