Gene expression of ulcer-associated cell lineage
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA521495 | ENA |
REPOSITORIES: ENA
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Project description:We applied RNA-seq analysis of total RNA isolated from laser capture microdissected intestinal epithelium. The analysis aimed at charactericing the gene expression seen in ulcer-associated cell lineage epithelial cells, and to contrast this with that of healthy control epithelium and epithelium from inflammatory bowel disease-patients with active inflammation.
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Project description:We investigate the changes between diabetic and non-diabetic wound healing process in chronic foot ulcer.
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Project description:Background & Aims: Spasmolytic polypeptide/TFF2-expressing metaplasia (SPEM) is known to emerge following parietal cell loss and during Helicobacter pylori infection, however its role in gastric ulcer repair is unknown. Therefore, we sought to investigate if SPEM plays a role in epithelial regeneration. Methods: Acetic acid ulcers were induced in young (2-3 months) C57BL/6 mice to determine the quality of ulcer repair. Gastric tissue was collected and analyzed to determine the expression of SPEM within the regenerating epithelium. As a comparison to native tissue the expression of SPEM was also identified within cultured gastric mouse-derived organoids. Results: Wound healing in the mice coincided with the emergence of SPEM expressing CD44v within the ulcerated region. The emergence of SPEM was also observed in cultured gastric organoids. Conclusions: These data demonstrate the SPEM may play a role in epithelial regeneration. Conclusions: These data demonstrate the SPEM may play a role in epithelial regeneration. 4 samples were used for ulcerated and uninjured tissue. 1 sample was used for intact tissue and organoid-derived RNA. The 'Ulcerated' samples represent C57BL/6 mice with ulcers and the 'Uninjured' samples represent the healthy controls (for "ulcerated" samples). The "Intact stomach tissue" and "Gastric organoids" samples are other types of samples that compared separately. "Gastric organoids" in this comparison are derived from "Intact stomach tissue".
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Project description:<p>Leg ulcers are among the most burdensome complications of sickle cell disease (SCD), yet the molecular determinants underlying ulcer susceptibility and recurrence remain incompletely characterized. We performed untargeted plasma lipidomics by LC–MS in 129 individuals with SCD from the REDS-III Brazil cohort, comparing participants with a recurrent sickle cell leg ulcer (SCLU) phenotype (n = 72) and SCD controls without ulcer history or follow-up episodes (n = 57). Data were split into a training set (80%; SCLUs n = 58, controls n = 46) and an independent validation set (20%; SCLUs n = 14, controls n = 11), with leakage-resistant preprocessing and variable selection restricted to the training set. After quality filtering, 2,419 features were retained. Univariate screening in the training set yielded 181 candidates, and 44 annotated metabolites were retained for visualization and modelling. Recurrent SCLUs showed higher lysophospholipids and oxylipins and lower sphingolipids and FAHFAs, consistent with inflammation, oxidative stress and membrane dysregulation. Random Forest achieved the best validation discrimination (AUC = 0.85; accuracy = 0.72; sensitivity = 0.86; specificity = 0.55). Untargeted plasma lipidomics defines an interpretable lipid signature linked to recurrent SCLUs and nominates candidates for targeted quantification and external validation to support individualized risk stratification.</p>
2025-12-19 | MTBLS13538 | MetaboLights
Project description:Background & Aims: Spasmolytic polypeptide/TFF2-expressing metaplasia (SPEM) is known to emerge following parietal cell loss and during Helicobacter pylori infection, however its role in gastric ulcer repair is unknown. Therefore, we sought to investigate if SPEM plays a role in epithelial regeneration. Methods: Acetic acid ulcers were induced in young (2-3 months) C57BL/6 mice to determine the quality of ulcer repair. Gastric tissue was collected and analyzed to determine the expression of SPEM within the regenerating epithelium. As a comparison to native tissue the expression of SPEM was also identified within cultured gastric mouse-derived organoids. Results: Wound healing in the mice coincided with the emergence of SPEM expressing CD44v within the ulcerated region. The emergence of SPEM was also observed in cultured gastric organoids. Conclusions: These data demonstrate the SPEM may play a role in epithelial regeneration. Conclusions: These data demonstrate the SPEM may play a role in epithelial regeneration.
2015-09-23 | GSE73336 | GEO
Project description:Chickarmane2008 - Stem cell lineage determination
In this work, a dynamical model of lineage
determination based upon a minimal circuit, as discussed in PMID: 17215298
, which contains the Oct4/Sox2/Nanog core as well its interaction
with a few other key genes is discussed.
This model is described in the article:
A computational model for understanding stem cell, trophectoderm and endoderm lineage determination.
Chickarmane V, Peterson C
PloS one. 2008, 3(10):e3478
Abstract:
BACKGROUND: Recent studies have associated the transcription factors, Oct4, Sox2 and Nanog as parts of a self-regulating network which is responsible for maintaining embryonic stem cell properties: self renewal and pluripotency. In addition, mutual antagonism between two of these and other master regulators have been shown to regulate lineage determination. In particular, an excess of Cdx2 over Oct4 determines the trophectoderm lineage whereas an excess of Gata-6 over Nanog determines differentiation into the endoderm lineage. Also, under/over-expression studies of the master regulator Oct4 have revealed that some self-renewal/pluripotency as well as differentiation genes are expressed in a biphasic manner with respect to the concentration of Oct4. METHODOLOGY/
PRINCIPAL FINDINGS: We construct a dynamical model of a minimalistic network, extracted from ChIP-on-chip and microarray data as well as literature studies. The model is based upon differential equations and makes two plausible assumptions; activation of Gata-6 by Oct4 and repression of Nanog by an Oct4-Gata-6 heterodimer. With these assumptions, the results of simulations successfully describe the biphasic behavior as well as lineage commitment. The model also predicts that reprogramming the network from a differentiated state, in particular the endoderm state, into a stem cell state, is best achieved by over-expressing Nanog, rather than by suppression of differentiation genes such as Gata-6.
CONCLUSIONS: The computational model provides a mechanistic understanding of how different lineages arise from the dynamics of the underlying regulatory network. It provides a framework to explore strategies of reprogramming a cell from a differentiated state to a stem cell state through directed perturbations. Such an approach is highly relevant to regenerative medicine since it allows for a rapid search over the host of possibilities for reprogramming to a stem cell state.
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2024-09-02 | BIOMD0000000209 | BioModels