Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Integrated Analysis of Laminin Subunit Beta 1 Impact on Subchorionic Hemorrhage: Insights into Inflammation and Thrombosis Pathways

ABSTRACT: Subchorionic hemorrhage (SCH) is characterized by a fluid-filled hypoechoic area in early pregnancy. This study investigates how laminin subunit β1 (LAMB1) modulates type III collagen (COL3A1) and Rac family small GTPase 1 (RAC1) in SCH coagulation and immunity.

ORGANISM(S): Homo Sapiens

SUBMITTER: Conghui Han

PROVIDER: PXD071504 | iProX | Wed Dec 03 00:00:00 GMT 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Similar Datasets

Targeting RAC1 as a novel strategy to reduce inflammation and liver damage in acute liver failure.

Project description:Background & Aims: The Rho GTPase RAC1 regulates key drivers of acute liver failure (ALF) such as oxidative stress and inflammation. The goal of this study was to determine the therapeutic potential of RAC1 pharmacological inhibition in ALF. Methods: The involvement of RAC1 in human ALF was explored by analyzing public transcriptome datasets. Murine models of ALF were induced by administration of either Concanavalin A, acetaminophen or D-Galactosamine/Lipopolysaccharide. In vitro assays were conducted on hepatocytes and macrophages primary cultures and cell lines. 1D-142 was used to explore the effect of RAC1 pharmacological inhibition. RNA-Seq analysis was performed and correlated with ALF human datasets to explore the therapeutic potential of RAC1 inhibition. Liver explants from patients with liver failure were treated in vitro with 1D-142. Results: RAC1-related pathways are upregulated in human ALF samples and correlate with immune activation and oxidative stress. Administration of 1D-142 ameliorated liver damage across all ALF murine models. 1D-142 treatment diminishes reactive oxygen species formation and reduces inflammatory cells migration and suppresses cytokine production both in vivo and in vitro. Transcriptome analysis of treated livers indicates that RAC1 pharmacological inhibition modulates dysregulated biological processes observed in ALF patients. Liver explants from ALF patients treated with 1D-142 exhibited reduced necrosis and reduced expression of pro-inflammatory genes. Conclusions: RAC1 plays a critical role in driving inflammation and oxidative stress in ALF. Targeted inhibition of RAC1 with 1D-142 protects against ALF in murine models; thus, RAC1 inhibition could be a potential therapeutic option for ALF.

2025-08-20 | GSE297179 | GEO

The effect of an NAT10 inhibitor (remodelin) on inflammation-related genes in the treatment of thalamic hemorrhage based on proteomics data

Project description:Thalamic hemorrhage is a disease caused by hemorrhage of the thalamic brain parenchyma and is accompanied by an inflammatory response during development. NAT10 has been associated with a wide range of diseases. The aim of this study was to explore the molecular mechanisms associated with the use of the NAT10 inhibitor (Remodelin) for the treatment of thalamic hemorrhage from an inflammatory perspective.

2025-02-24 | PXD058910 | Pride

Project description:Isobaric labeling quantitative phospho proteomics uncovered differential site-specific protein phosphorylation within mTOR, Rho GTPase and MAPK systems in platelets from aged donors. Western blot confirmed constitutive activation of the mTOR pathway in platelets from both aged humans and mice, which was associated with increased aggregation compared to young controls. Inhibition of mTOR either with Torin 1 in aged humans, or genetic deletion in aged mice, reversed platelet hyperreactivity. Mechanistically, we noted increased levels of mitochondrial reactive oxygen species and Rac1 activation in resting platelets from aged mice, as well as increased p38 phosphorylation upstream of thromboxane generation following agonist stimulation.

2025-05-25 | PXD049967 | Pride

Neutrophils after mouse subarachnoid hemorrhage

Project description:Subarachnoid hemorrhage causes an increase in inflammation and may effect neutrophils. Here, we test if there are differences in expression from neutrophils after subarachnoid hemorrhage in mice on days 1 and 3 (compared with a sham control).

2025-10-24 | GSE216572 | GEO

Examining Transcriptomic Alterations in Rat Models of Intracerebral Hemorrhage and Severe Intracerebral Hemorrhage

Project description:Intracerebral hemorrhage (ICH) is a life-threatening condition associated with significant morbidity and mortality. Understanding the molecular mechanisms underlying ICH and its severe form is crucial for developing effective therapeutic strategies. This study investigates transcriptomic alterations in rodent models of ICH and severe intracerebral hemorrhage to shed light on the genetic pathways involved in hemorrhagic brain injury. We performed principal component analysis, revealing distinct principal component segments of normal rats compared to intracerebral hemorrhage and severe intracerebral hemorrhage rats. We further employed heatmaps and volcano plots to identify differentially expressed genes and utilized bar plots and KEGG pathway analysis to elucidate the different molecular pathways involved. Using comprehensive RNA sequencing and bioinformatics analyses, we identified a multitude of differentially expressed genes in both the ICH and severe ICH models. Our results revealed 5679 common genes among the normal, intracerebral hemorrhage, and severe intracerebral hemorrhage groups in the upregulated genes group, and 1196 common genes in the downregulated genes. A volcano plot comparing the groups further highlighted common genes, including PDPN, TIMP1, SERPINE1, TUBB6, and CD44. These findings underscore the complex interplay of genes involved in inflammation, oxidative stress, and neuronal damage. Furthermore, pathway enrichment analysis uncovered key signaling pathways, including the TNF signaling pathway, protein processing in the endoplasmic reticulum, MAPK signaling pathway, and Fc gamma R-mediated phagocytosis, implicated in the pathogenesis of ICH.

2024-06-11 | GSE264394 | GEO

The effect of an NAT10 inhibitor (remodelin) on inflammation-related genes in the treatment of thalamic hemorrhage based on RNA sequencing data

2025-11-11 | GSE275066 | GEO

Identification of inflammation-related microRNAs deregulated in the plasma from intracerebral hemorrhage patients

Project description:We tested the hypothesis that circulating microRNAs (miRNAs) present in plasma might display a specific signature in patients with intracerebral hemorrhage (ICH). Global miRNA profiles were determined with the Agilent Human miRNA Microarray platform, 027233. ICH patients display a characteristic inflammation-related miRNA profile as compared to healthy controls. Plasma samples were collected from the following 6 subject groups: male ICH patients (n=8), female ICH patients (n=7), male healthy control (n=4), female healthy control (n=4), male ischemic stroke patients (n=8) and female ischemic stroke patients (n=8). Total RNAs isolated from 1 ml plasma were pooled for each group. A fixed volume of RNA sample was withdrawn from each pool and used for microarray detection.

2013-01-19 | E-GEOD-43618 | biostudies-arrayexpress

Identification of inflammation-related microRNAs deregulated in the plasma from intracerebral hemorrhage patients

2013-01-19 | GSE43618 | GEO

Gut microbiota dysbiosis and neurological function recovery after intracerebral hemorrhage [16S rRNA-Seq]

Project description:We aimed to investigate the microbial community composition in patients with intracerebral hemorrhage (ICH) and its effect on prognosis. The relationship between changes in bacterial flora and the prognosis of spontaneous cerebral hemorrhage was studied in two cohort studies. Fecal samples from healthy volunteers and patients with intracerebral hemorrhage were subjected to 16S rRNA sequencing at three time points: T1 (within 24 hours of admission), T2 (3 days post-surgery), and T3 (7 days post-surgery) using Illumina high-throughput sequencing technology.

2024-08-22 | E-MTAB-14351 | biostudies-arrayexpress

Protein kinase 7 regulating extracellular matrix assemblies and intracellular RAC1 and myosin II activities in the mesenchyme is important to Wolffian duct morphogenesis.

Project description:Wolffian/epididymal duct morphogenesis highly coordinates with its specialized function of providing microenvironment for sperm maturation. Without normal development of Wolffian duct, male infertility will result. Therefore, it is important to understand the cellular and molecular mechanisms that regulated Wolffian duct morphogenesis. Our previous study showed that mediolateral intercalation of epithelial cells was a major driver of ductal elongation. In addition, radial intercalation of mesenchymal cells surrounding the duct also played roles in Wolffian duct morphogenesis, and all of these cell re-arrangements were regulated by protein tyrosine kinase 7 (PTK7), a member of the planar cell polarity (PCP) non-canonical Wnt pathway. In this study, we showed that PTK7 regulated assemblies of extracellular matrix (ECM) at the basement membrane and throughout the mesenchyme. Abnormal assembly of laminin, collagen IV, and nephronectin at the basement membrane and fibrosis-like deposition of fibrilla collagen in the interstitium were observed in Ptk7 knockout Wolffian ducts. Meanwhile, PTK7 regulated activity levels of small GTPase RAC1 and myosin II in the mesenchyme of the Wolffian duct. Activity levels of RAC1 and myosin II decreased in the Ptk7 knockout mesenchyme compared to controls. When in-vitro-cultured Wolffian ducts were treated with collagenase IV, cross-link of fibrilla collagen was reduced, Wolffian duct elongation and coiling was reduced significantly, and cyst-like bulge was developed in the epithelial duct. When Wolffian ducts were treated with RAC1 inhibitor NSC23766, fibrilla collagen in the mesenchyme was disassembled, and Wolffian duct elongation was suppressed significantly. Our finding suggested that PTK7 regulated ECM assembly in the mesenchyme likely through regulating RAC1 and myosin II activities. Dynamic assembly and remodeling of ECM were important to Wolffian duct morphogenesis.

2018-05-09 | GSE98715 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data