RNA-Seq of fibrillin 1 (Fbn1) tight-skin (Tsk) mice
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA737339 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14803578.fastq.gz | Fastqsanger.gz | |||
| SRR14803579.fastq.gz | Fastqsanger.gz | |||
| SRR14803580.fastq.gz | Fastqsanger.gz | |||
| SRR14803581.fastq.gz | Fastqsanger.gz | |||
| SRR14803582.fastq.gz | Fastqsanger.gz |
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Project description:A fibrotic environment supports cancer growth. Our aim is to assess the transcriptomic differences by performing RNA sequencing in a fibrosis mouse model to provide insight into the increased growth of ovarian cancer in Fbn1 Tsk mice. Elucidating the targets important in fibrosis could provide potential clues to the mechanism of preferential cancer growth in fibrotic environments.
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Project description:Patients with systemic sclerosis have a significantly increased incidence of developing various solid malignancies within a few years of systemic sclerosis onset but the mechanism of tumor promotion is not well understood. The tight skin (TSK) mouse has been a valuable model for investigating systemic sclerosis-related pathologies due to increased extracellular matrix deposition, fibrosis in connective tissues, and altered immune cell activation. Despite the role of extracellular matrix and fibrosis in cancer progression, the potential of the TSK mouse as a model for cancer studies is unexplored. Our RNA sequencing analysis of adult dorsal skin samples from TSK and wild-type (WT) mice revealed a notable enrichment for genes typically associated with cancer aggressiveness and desmoplasia. To investigate the impact of the altered microenvironment in TSK mice on cancer progression, we compared the tumor-forming capabilities in TSK mice and WT mice using a syngeneic mouse model of ovarian cancer. TSK mice exhibited larger and more invasive subcutaneous and intraperitoneal tumors in comparison to WT controls, suggesting the role of the microenvironment in promoting cancer progression. Single-cell RNA sequencing analysis of tumors in TSK and WT mice revealed a higher neutrophil-to-lymphocyte ratio, and an enrichment in profibrotic subpopulations of myofibroblasts and macrophages in TSK mice.
2024-04-08 | GSE255493 | GEO
Project description:Patients with systemic sclerosis have a significantly increased incidence of developing various solid malignancies within a few years of systemic sclerosis onset but the mechanism of tumor promotion is not well understood. The tight skin (TSK) mouse has been a valuable model for investigating systemic sclerosis-related pathologies due to increased extracellular matrix deposition, fibrosis in connective tissues, and altered immune cell activation. Despite the role of extracellular matrix and fibrosis in cancer progression, the potential of the TSK mouse as a model for cancer studies is unexplored. Our RNA sequencing analysis of adult dorsal skin samples from TSK and wild-type (WT) mice revealed a notable enrichment for genes typically associated with cancer aggressiveness and desmoplasia. To investigate the impact of the altered microenvironment in TSK mice on cancer progression, we compared the tumor-forming capabilities in TSK mice and WT mice using a syngeneic mouse model of ovarian cancer. TSK mice exhibited larger and more invasive subcutaneous and intraperitoneal tumors in comparison to WT controls, suggesting the role of the microenvironment in promoting cancer progression. Single-cell RNA sequencing analysis of tumors in TSK and WT mice revealed a higher neutrophil-to-lymphocyte ratio, and an enrichment in profibrotic subpopulations of myofibroblasts and macrophages in TSK mice.
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Project description:Myxomatous valve disease is the most common form of heart valve disease leading to morbidity and mortality worldwide. It is primarily associated with inherited connective tissue disorders caused by genetic variants in extracellular matrix genes such as Marfan syndrome. Mice with Fibrillin 1 gene variant Fbn1 C1039G/+ recapitulate histopathological features of Marfan syndrome. However, the cell heterogeneity and changes of gene expression at single cell level in Marfan syndrome valves are completed unknown.
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Project description:Fibrillin-1 (FBN1) is the major component of extracellular matrix microfibrils, which are required for proper development of elastic tissues including heart and lung. Through protein-protein interactions with latent TGF-beta binding protein 1 (LTBP1), microfibrils assist regulation of TGF-beta signaling. Mutations within the 47 epidermal growth factor-like (EGF) repeats of FBN1 cause autosomal dominant disorders including Marfan Syndrome that disrupt TGF-beta signaling. We recently identified 2 novel protein O-glucosyltransferases, Protein O-glucosyltransferase 2 (POGLUT2) and Protein O-glucosyltransferase 3 (POGLUT3), that modify a few EGF repeats on Notch. Here, using mass spectral analysis, we show that POGLUT2 and POGLUT3 also modify over half of the EGF repeats on FBN1, fibrillin-2 (FBN2), and LTBP1. While most sites are modified by both enzymes, some sites show a preference for either POGLUT2 or POGLUT3. POGLUT2 and POGLUT3 are homologs of POGLUT1, which stabilizes Notch proteins by addition of O-glucose to Notch EGF repeats. Like POGLUT1, POGLUT2 and 3 can discern a folded versus unfolded EGF repeat, suggesting POGLUT2 and 3 are involved in a protein folding pathway. In vitro secretion assays using recombinant FBN1 revealed reduced FBN1 secretion in POGLUT2 knockout, POGLUT3 knockout, and POGLUT2 and 3 double knockout HEK293T cells compared to wild type. These results illustrate that POGLUT2 and 3 function together to O-glycosylate protein targets, and that these modifications play a role in secretion of target proteins.
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Project description:Mitral valves were isolated from 2-month-old mice with the following 4 genotypes: 1) CCR2 RFP/+ (Chet), 2) CCR2 RFP/RFP (Cko), 3) Fbn1 C1039G/+; CCR2 RFP/+ (FhetChet), 4) Fbn1 C1039G/+; CCR2 RFP/RFP (FhetCko). N=4 for each genotype. Total RNA was extracted from mitral valves individually for gene expression profiling.
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Project description:We used microarrays to characterize the global changes in gene expression within the ascending aorta of mice due to conditional disruption of TGF-M-NM-2 signaling in smooth muscle and/or due to heterozygous fibrillin-1 mutation. Myh11-CreERT2.Tgfbr2f/f (abbreviated as Cre.Tgfbr2) mice were cross-bred to Fbn1C1039G/+ (abbreviated as Fbn1C/+) mice and treated with vehicle or tamoxifen for 5 d starting at 4 wk of age to generate 4 groups of animals: 1) Cre.Tgfbr2-Veh: controls with intact TGF-M-NM-2 signaling and wild-type fibrillin-1 expression; 2) Cre.Tgfbr2-Tmx: conditional disruption of Tgfbr2 in smooth muscle with wild-type fibrillin-1 expression; 3) Fbn1C1039G.Cre.Tgfbr2-Veh: heterozygous expression of mutant fibrillin-1 with intact TGF-M-NM-2 signaling; and 4) Fbn1C1039G.Cre.Tgfbr2-Tmx: conditional disruption of Tgfbr2 in smooth muscle with heterozygous expression of mutant fibrillin-1. The animals were euthanized at 6 weeks of age and their ascending aortas (from above the coronary arteries to the first arch branch) were collected and total RNA was extracted.
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Project description:Draft Genome Sequence of Desulforhabdus sp. strain TSK
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Project description:Mammalian skeletal muscle contains heterogenous myofibers with different contractile and metabolic properties that sustain muscle mass and endurance capacity. The transcriptional regulators that govern these myofiber gene programs have been elucidated. However, the hormonal cues that direct the specification of myofiber types and muscle endurance remain largely unknown. Here we uncover the secreted factor Tsukushi (TSK) as an extracellular signal that is required for maintaining muscle mass, strength, and endurance capacity, and contributes to muscle regeneration. Mice lacking TSK exhibited reduced grip strength and impaired exercise capacity. Muscle transcriptomic analysis revealed that TSK deficiency results in a remarkably selective impairment in the expression of myofibrillar genes characteristic of slow-twitch muscle fibers that is associated with abnormal neuromuscular junction formation. AAV-mediated overexpression of TSK failed to rescue these myofiber defects in adult mice, suggesting that the effects of TSK on myofibers are likely restricted to certain developmental stages. Finally, mice lacking TSK exhibited diminished muscle regeneration following cardiotoxin-induced muscle injury. These findings support a crucial role of TSK as a hormonal cue in the regulation of contractile gene expression, endurance capacity, and muscle regeneration.
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Project description:Dietary glucosylceramide (GC) improves skin barrier function. To elucidate the molecular mechanisms involved, we used a microarray system to analyze mRNA expression in SDS-treated dorsal skin of hairless mouse. Transepidermal water loss of mouse skin was increased by SDS treatment and the increase was significantly reduced by prior oral administration of glucosylceramides. Microarray-evaluated mRNA expression ratios showed statistically significant increase of expression of genes related to cornified envelope and tight junction formation versus all genes in glucosylceramide-fed/SDS-treated mouse skin. We then examined the contribution of glucosylceramide metabolites to tight junction formation of cultured keratinocytes. SDS treatment of cultured keratinocytes significantly decreased the transepidermal electrical resistance, and the decrease was significantly ameliorated in the presence of sphingosine or phytosphingosine, the major metabolites of glucosylceramide. These results suggest that oral administration of glucosylceramide improves skin barrier function by upregulating genes associated with both cornified envelope and tight junction formation. Two-condition experiment, effect of oral intake of GC on mice skin before SDS treatment (0d), and after SDS treatment(2d), Biological replicates: 3 replicates for 0d, 4 replicates for 2d.
2012-03-31 | E-GEOD-28086 | biostudies-arrayexpress