Transcriptomic analysis of the livers of Bnc2 heterozygous or wild-type mice fed with a pro-fibrogenic NASH diet
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE185527 | GEO | 2022/08/07
REPOSITORIES: GEO
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Project description:Transient angiotensin converting enzyme (ACE) inhibition in spontaneously hypertensive rats (SHR) protects against future injury-induced cardiac inflammation, fibrosis, and dysfunction. Here, we used single cell RNA sequencing (scRNA-Seq) to test the hypothesis that transient ACE inhibitor treatment would induce a persistent shift in hypertensive cardiac fibroblast subpopulations. Adult male SHRs (11 weeks old) were treated for 2 weeks with an ACE inhibitor, enalapril (30mg/kg/day, p.o.), or water (control) followed by a 2-week washout period (n=7/group). Cardiac fibroblasts were isolated from the left ventricle and subjected to scRNA-Seq. Nine clusters of fibroblasts (numbered 0-8) were identified with 98% of cells clustering into subsets 0-6. Transient treatment produced significant changes within and across clusters. Cluster 1 depicted the highly fibrogenic gene profile, with cluster 6 serving as a gateway to cluster 1. Transient ACE inhibition depleted the gateway and expanded cluster 0, which was the least fibrogenic profile. Moreover, within cluster 1 fibroblasts, ACE inhibition reduced expression of individual fibrosis genes (e.g. COL1A1, COL3A1, and FN1; all p<0.05). Clusters 2-5 reflected proliferative, moderately fibrogenic, translationally active, and lowly inflammatory subsets of fibroblasts, all of which exhibit attenuated fibrogenic gene expression after transient ACE inhibition. In conclusion, transient ACE inhibition shifts cardiac fibroblast subpopulations and degree of activation resulting in an overall reduced fibrogenic phenotype.
2020-10-01 | GSE155699 | GEO
Project description:Preservation of cell identity is necessary for homeostasis of most adult tissues. This process is challenged every time a tissue undergoes regeneration after stress or injury. In the lethal Duchenne muscular Dystrophy (DMD), skeletal muscle regenerative capacity declines gradually as fibrosis increases. Using genetically engineered-tracing mice, we demonstrate that in dystrophic muscle, specialized cells of muscular, endothelial and hematopoietic origins gain plasticity towards a fibrogenic fate via a TGFβ-mediated pathway. This results in loss of cellular identity and normal function, with deleterious consequences for regeneration. Furthermore, this fibrogenic process involves acquisition of a mesenchymal progenitor multipotent status, illustrating a link between fibrogenesis and gain of progenitor cell functions. As this plasticity was also observed in DMD patients, we propose that mesenchymal transitions impair regeneration and worsen diseases with a fibrotic component. TGFb exposure induced gene expression was measured after 4 days of treatment compared to untreated cells. Three independent experiments were performed both for the treatment and for the control
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Project description:Preservation of cell identity is necessary for homeostasis of most adult tissues. This process is challenged every time a tissue undergoes regeneration after stress or injury. In the lethal Duchenne muscular Dystrophy (DMD), skeletal muscle regenerative capacity declines gradually as fibrosis increases. Using genetically engineered-tracing mice, we demonstrate that in dystrophic muscle, specialized cells of muscular, endothelial and hematopoietic origins gain plasticity towards a fibrogenic fate via a TGFβ-mediated pathway. This results in loss of cellular identity and normal function, with deleterious consequences for regeneration. Furthermore, this fibrogenic process involves acquisition of a mesenchymal progenitor multipotent status, illustrating a link between fibrogenesis and gain of progenitor cell functions. As this plasticity was also observed in DMD patients, we propose that mesenchymal transitions impair regeneration and worsen diseases with a fibrotic component.
2015-04-09 | GSE67687 | GEO
Project description:The Long Evans/orl (LE/orl) rat is an animal model of inherited undescended testis (UDT). To explore genetic mechanisms of UDT, we studied differential gene expression in LE/orl and LE wild type (LE/wt) fetal gubernaculum and testis. Analyses of differentially expressed probe sets linked below as supplementary files:; Analysis_methods.txt [A description of the analysis]; gub.txt [Genes differentially expressed in between wt and orl gubernacula]; testes.txt [Genes differentially expressed between wt and orl testes]; wt.txt [Genes differentially expressed in wt gubernacular development] Experiment Overall Design: Fetuses were harvested from timed matings of LE/wt and LE/orl rats at gestational day (GD) 17, 18, 19, and 20. Single gubernaculum and testis were removed from male fetuses and total RNA was isolated from each organ. Left organs were used, except for GD 20 fetuses where both right and left gubernacula were included. For female fetuses, the right and left gubernacula from a single fetus were pooled before RNA isolation. A total of 54 samples were hybridized to GeneChips; 34 gubernacular samples and 20 testes samples. There were 13 sample groups, each included biological replicate arrays. The sample groups were (1) female LE/wt GD18 gubernacula n=4, (2) male LE/wt GD18 left gubernacula n=4, (3) male LE/wt GD19 left gubernacula n=4, (4) male LE/wt GD20 left gubernacula n=4, (5) male LE/wt GD20 right gubernacula n=3, (6) male LE/orl GD18 left gubernacula n=4, (7) male LE/orl GD19 left gubernacula n=4, (8) male LE/orl GD20 left gubernacula n=4, (9) male LE/orl GD20 right gubernacula n=3, (10) male LE/wt GD17 left testes n=5, (11) male LE/wt GD19 left testes n=5, (12) male LE/orl GD17 left testes n=5, and (13) male LE/orl GD19 left testes n=5.
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Project description:The Long Evans/orl (LE/orl) rat is an animal model of inherited undescended testis (UDT). To explore genetic mechanisms of UDT, we studied differential gene expression in LE/orl and LE wild type (LE/wt) fetal gubernaculum and testis. Analyses of differentially expressed probe sets linked below as supplementary files: Analysis_methods.txt [A description of the analysis] gub.txt [Genes differentially expressed in between wt and orl gubernacula] testes.txt [Genes differentially expressed between wt and orl testes] wt.txt [Genes differentially expressed in wt gubernacular development] Keywords: strain/condition predisposition, disease state analysis, developmental
2008-02-03 | GSE7755 | GEO
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