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.
2019-04-01 | GSE126299 | GEO
Project description:Marjolin’s Ulcer is an aggressive cutaneous malignancy that typically ensues over a period of time in the post-burned lesions and scars or any other chronic wound. Marjolin’s Ulcer makes up 1.2% of all skin cancers, it is reported that 2% of squamous cell carcinoma and 0.03% of basal cell carcinoma originate in burn scars. Recent studies have shown that long non-coding (lncRNA) plays critical roles in a myriad of biological processes and human diseases,Since the roles of lncRNA in Marjolin’s Ulcer remain unknown,they were investigated in the study.Our findings indicate that the expression profiles of lncRNAs has changed in Marjolin’s Ulcer as compared with normal skin and para-cancerous scar, and may provide novel insight into the molecular mechanism underlying the disease and potential novel diagnostic or therapeutic targets for Marjolin’s Ulcer.
2018-12-11 | GSE110138 | GEO
Project description:We investigate the changes between diabetic and non-diabetic wound healing process in chronic foot ulcer.
2023-02-01 | GSE223964 | GEO
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".
2015-09-23 | E-GEOD-73336 | biostudies-arrayexpress
Project description:We investigate the changes between diabetic and non-diabetic wound healing process in chronic foot ulcer.
2023-10-24 | GSE245703 | GEO
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.
This model is hosted on BioModels Database
and identified
by: MODEL8390025091
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
2008-12-05 | BIOMD0000000209 | BioModels
Project description:Hematopoietic stem cells (HSCs) must balance self-renewal and lineage differentiation to regenerate the hematopoietic system throughout life. HSCs exhibit lineage-associated gene expression that keeps them responsive to demands of mature blood production. However, it is not known whether this process, termed lineage priming, directly influences HSC self-renewal. We investigated the link between stemness and lineage priming by attenuating the early lymphoid transcription factor E47 through ID2 over-expression (OE). Transcriptional profiling of ID2 OE HSCs showed down regulation of B-cell factors including EBF1 and FOXO1 with a concomitant increase in stemness programs and myeloerythroid factors including CEBPA and GATA1. This resulted in myeloid commitment bias from the earliest stages of differentiation. HSC self-renewal was strongly affected by this lineage perturbation resulting in an 11-fold expansion of HSCs. Thus, early lymphoid transcription factors antagonize human HSC self-renewal, providing a direct link between differentiation program priming and the maintenance of stem cell self-renewal. Three independent lineage depleted CB samples were transduced with P-CTRL or P-ID2 and injected into 5 mice (30 mice total). From every group of 5 mice, human lin- cells were isolated and GFP+CD34+CD38-CD45RA- HSPCs were sorted by FACS.
2013-12-01 | E-GEOD-45486 | biostudies-arrayexpress
Project description:Chickarmane2008 - Stem cell lineage - NANOG GATA-6 switch
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.
This model is hosted on BioModels Database
and identified
by: MODEL8389825246
.
To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource
for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to the public
domain worldwide. Please refer to CC0 Public Domain
Dedication
for more information.
2008-12-05 | BIOMD0000000210 | BioModels
Project description:Background. The mechanisms by which environmental risk factors (eg, stress) predispose to symptoms and gastric emptying (GE) disturbances in non-ulcer dyspepsia (NUD) is unknown. Our aims were to compare the circulating leukocytes’ epigenome between NUD patients with normal versus delayed and normal versus rapid GE. Methods. In 24 NUD patients, we evaluated gastrointestinal symptoms, GE (scintigraphy) and 3 promoter/enhancer-associated histone modifications (H3K4me3, H3K9ac, and H3K27ac) by chromatin immunoprecipitation-sequencing in buffy coats, then compared the genome-wide binding of histone marks between patients with normal versus delayed and normal versus rapid GE. Key results. GE was normal (9 patients), delayed (6 patients), or rapid (9 patients). Compared to normal GE, there was differential binding of H3K4me3, which marks active promoters, at 100 genes in delayed and 233 genes in rapid GE (FDR < 0.05). Delayed GE was associated with increased H3K4me3 binding at several genes that regulate T cell functions (eg, CD247, IL2RA, CD69, CD96, ICOS, ITK, and GRAP2); conversely, binding was reduced at genes that regulate neuronal synapses (ie, SYT6, SYT12, CDH2, CDH11, EFNB3, CAMK2B, and SHISA6) and neuronal nitric oxide synthase (NOS1). In rapid GE, genes related to opioid signaling (OPRD1, MAPK4, CAMK2B, and PDE1C), neuronal development, and synaptic functions bound less H3K4me3. No or few genes were differentially enriched with H3K9ac and H3K27ac. Conclusions. H3K4me3 discriminates among patients with normal, rapid, and delayed GE. Delayed GE is associated with alterations that suggest increased T-cell functions. Rapid GE is associated with changes suggesting reduced opioid signaling.
2021-12-26 | GSE139166 | GEO