Overactivation of wound healing-associated TGF-beta responses in EZH2-deficient decidual stromal cells.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA720660 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14189405.fastq.gz | Fastqsanger.gz | |||
| SRR14189406.fastq.gz | Fastqsanger.gz | |||
| SRR14189407.fastq.gz | Fastqsanger.gz | |||
| SRR14189408.fastq.gz | Fastqsanger.gz | |||
| SRR14189409.fastq.gz | Fastqsanger.gz |
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Project description:Our objective was to identify genes upregulated by TGF-beta in control and Ezh2 cKO decidual stromal cells (DSCs), and to compare this set of genes with a previously identified gene set of H3K27me3-marked decidual genes that are putatively silenced by EZH2/PRC2 (Nancy et al. JCI. 2018). We also wanted to assess baseline (BL) gene expression in control and Ezh2 cKO DSCs, and compare it to an RNA-seq analysis of differential gene expression in whole tissue Ezh2 cKO and control decidua. RNA was isolated from untreated and TGF-beta treated decidual stromal cells from control and Ezh2 cKO mice. Sequencing provided was 706 million total reads with an average of 82.2% of these reads aligning uniquely to the mouse genome. Reads uniquely mapped to known mRNAs were used to identify gene expression changes between housing conditions using DESeq2. TGF-beta induced 638 protein-coding genes in EZH2-deficient DSCs versus 480 in control DSCs (with a 295 gene overlap), demonstrating that EZH2-deficient DSCs are transcriptionally more responsive to TGF- (P=0.0025, Fisher’s exact test). Within the 638 genes, activated fibroblast signature genes were highly over-represented. TGF-target genes were 2.7-fold over-represented within the set of genes with higher expression in EZH2-deficient DSCs at baseline (BL; i.e., when neither EZH2-deficient nor control DSCs were treated with TGF-beta; P<1x10-20) . 741 genes were overexpressed in Ezh2 cKO DSCs compared to control DSCs, and 904 genes were underexpressed. Moreover, by comparing to our laboratory's previous CHIP-Seq analysis (Nancy et al. JCI 2018), we noted that genes overexpressed in cKO mice were enriched in previously identified H3K27me3-marked genes (P<1x10-26).
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Project description:This a model from the article:
Macrophage dynamics in diabetic wound dealing.
Waugh HV, Sherratt JA. Bull Math Biol
2006 Jan;68(1):197-207 16794927
,
Abstract:
Wound healing in diabetes is a complex process, characterised by a chronic
inflammation phase. The exact mechanism by which this occurs is not fully
understood, and whilst several treatments for healing diabetic wounds exist,
very little research has been conducted towards the causes of the extended
inflammation phase. We describe a mathematical model which offers a possible
explanation for diabetic wound healing in terms of the distribution of
macrophage phenotypes being altered in the diabetic patient compared to normal
wound repair. As a consequence of this, we put forward a suggestion for
treatment based on rectifying the macrophage phenotype imbalance.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Waugh HV, Sherratt JA. (2006) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
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
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In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
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Project description:Diabetic foot ulcers (DFU) are one of the major complications in type II diabetes patients and can result in amputation and morbidity. Although multiple approaches are used clinically to help wound closure, many patients still lack adequate treatment. Here we show that IL-20 subfamily cytokines are upregulated during normal wound healing. While there is a redundant role for each individual cytokine in this subfamily in wound healing, mice deficient in IL-22R, the common receptor chain for IL-20, IL-22, and IL-24, display a significant delay in wound healing. Furthermore, IL-20, IL-22 and IL-24 are all able to promote wound healing in type II diabetic db/db mice. When compared to other growth factors such as VEGF and PDGF that accelerate wound healing in this model, IL-22 uniquely induced genes involved in reepithelialization, tissue remodeling and innate host defense mechanisms from wounded skin. Interestingly, IL-22 treatment showed superior efficacy compared to PDGF or VEGF in an infectious diabetic wound model. Taken together, our data suggest that IL-20 subfamily cytokines, particularly IL-20, IL-22, and IL-24, might provide therapeutic benefit for patients with DFU.
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