Autocrine Sfrp1 inhibits fibroblast invasion during transition to injury induced myofibroblasts - Tcf21 labeled mice
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ABSTRACT:
PROVIDER: PRJNA856687 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20023200_1.fastq.gz | Fastqsanger.gz | |||
| SRR20023200_2.fastq.gz | Fastqsanger.gz | |||
| SRR20023201_1.fastq.gz | Fastqsanger.gz | |||
| SRR20023201_2.fastq.gz | Fastqsanger.gz | |||
| SRR20023202_1.fastq.gz | Fastqsanger.gz |
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Project description:Fibroblast to myofibroblast conversion is a major driver of tissue remodeling in organ fibrosis. Here, we combined spatial transcriptomics, longitudinal single-cell RNA-seq and genetic lineage tracing to study fibroblast fates during mouse lung regeneration. We discovered a transitional fibroblast state characterized by high Sfrp1 expression, derived from both Tcf21-Cre lineage positive and negative cells. Sfrp1+ cells appeared early after injury in peribronchiolar, adventitial and alveolar locations and preceded the emergence of myofibroblasts. We identified lineage specific paracrine signals and inferred converging transcriptional trajectories towards Sfrp1+ transitional fibroblasts and Cthrc1+ myofibroblasts. Tgfβ1 downregulated Sfrp1 in non-invasive transitional cells and induced their switch to an invasive Cthrc1+ myofibroblast identity. Our study reveals the convergence of spatially and transcriptionally distinct fibroblast lineages into transcriptionally uniform myofibroblasts and identifies Sfrp1 as an autocrine inhibitor of fibroblast invasion during early stages of fibrogenesis.
2024-02-15 | GSE207687 | GEO
Project description:Fibroblast to myofibroblast conversion is a major driver of tissue remodeling in organ fibrosis. Several distinct lineages of fibroblasts support homeostatic tissue niche functions, yet, specific activation states and phenotypic trajectories of fibroblasts during injury repair have remained unclear. Here, we combined spatial transcriptomics, longitudinal single-cell RNA-seq and genetic lineage tracing to study fibroblast fates during mouse lung regeneration. We discovered a transitional fibroblast state characterized by high Sfrp1 expression, derived from both Tcf21-Cre lineage positive and negative cells. Sfrp1+ cells appeared early after injury in peribronchiolar, adventitial and alveolar locations and preceded the emergence of myofibroblasts. We identified lineage specific paracrine signals and inferred converging transcriptional trajectories towards Sfrp1+ transitional fibroblasts and Cthrc1+ myofibroblasts. Tgfβ1 downregulated Sfrp1 in non-invasive transitional cells and induced their switch to an invasive Cthrc1+ myofibroblast identity. Finally, using loss of function experiments we show that autocrine Sfrp1 directly inhibits fibroblast invasion by regulating the RhoA pathway. In summary, our study reveals the convergence of spatially and transcriptionally distinct fibroblast lineages into transcriptionally uniform myofibroblasts and identifies Sfrp1 as an autocrine inhibitor of fibroblast invasion during early stages of fibrogenesis.
2023-11-14 | GSE207561 | GEO
Project description:Fibroblast to myofibroblast conversion is a major driver of tissue remodeling in organ fibrosis. Here, we combined spatial transcriptomics, longitudinal single-cell RNA-seq and genetic lineage tracing to study fibroblast fates during mouse lung regeneration. We discovered a transitional fibroblast state characterized by high Sfrp1 expression, derived from both Tcf21-Cre lineage positive and negative cells. Sfrp1+ cells appeared early after injury in peribronchiolar, adventitial and alveolar locations and preceded the emergence of myofibroblasts. We identified lineage specific paracrine signals and inferred converging transcriptional trajectories towards Sfrp1+ transitional fibroblasts and Cthrc1+ myofibroblasts. Tgfβ1 downregulated Sfrp1 in non-invasive transitional cells and induced their switch to an invasive Cthrc1+ myofibroblast identity. Our study reveals the convergence of spatially and transcriptionally distinct fibroblast lineages into transcriptionally uniform myofibroblasts and identifies Sfrp1 as an autocrine inhibitor of fibroblast invasion during early stages of fibrogenesis.
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Project description:Autocrine Sfrp1 inhibits lung fibroblast invasion during transition to injury induced myofibroblasts
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Project description:Autocrine Sfrp1 inhibits fibroblast invasion during transition to injury induced myofibroblasts - daily profiling of mouse lungs after Bleomycin injury
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Project description:Microarray data to accompany Gauger et al. (2009) Cancer Cell International paper A treated X untreated design was used whereby immortalized human mammary epithelial cell lines (TERT cells) were modified to stably express an siRNA that knocked down SFRP1 expression. These "treated" cells were labeled with Cy5 and four replicate harvests were hybridized to Agilent 4by44k whole genome microarrays, along with a Cy3 labeled untreated control. The untreated control consisted of 4 pooled harvests of the parent cell line in normal growth conditions at 60-80% confluence.
2010-05-08 | E-GEOD-15948 | biostudies-arrayexpress
Project description:Cardiac fibroblasts convert to myofibroblasts with injury to mediate healing after acute myocardial infarction and to mediate long-standing fibrosis with chronic disease. Myofibroblasts remain a poorly defined cell-type in terms of their origins and functional effects in vivo. Methods: Here we generate Postn (periostin) gene-targeted mice containing a tamoxifen inducible Cre for cellular lineage tracing analysis. This Postn allele identifies essentially all myofibroblasts within the heart and multiple other tissues. Results: Lineage tracing with 4 additional Cre-expressing mouse lines shows that periostin-expressing myofibroblasts in the heart derive from tissue-resident fibroblasts of the Tcf21 lineage, but not endothelial, immune/myeloid or smooth muscle cells. Deletion of periostin+ myofibroblasts reduces collagen production and scar formation after myocardial infarction. Periostin-traced myofibroblasts also revert back to a less activated state upon injury resolution. Conclusions: Our results define the myofibroblast as a periostin-expressing cell-type necessary for adaptive healing and fibrosis in the heart, which arises from Tcf21+ tissue-resident fibroblasts. Fluidigm C1 whole genome transcriptome analysis of lineage mapped cardiac myofibroblasts
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Project description:All samples are conditioned media from primary cultured human gastric myofibroblasts, derived from either carcinoma tissue, or adjacent non cancerous tissue. In each experiment the cancer-derived myofibroblasts are compared against the non-cancer derived myofibroblasts from the same patient. All of the experiments were samples from Patient 1, except for 648, which is from Patient 2. SILAC labelling in each case is; 567 - Methionine COFRADIC; Cancer-derived = Heavy, Non-cancer = Light 575 - N-terminal COFRADIC; Cancer-derived = Heavy, Non-cancer = Light 646 - Cancer-derived = Light, Non-cancer = Heavy 647 - Non-cancer = Heavy, Non-cancer = Light (same cell line labelled twice to create a control experiment) 648 - Cancer-derived = Heavy, Non-cancer = Light
2013-06-20 | PRD000744 | Pride
Project description:The aim of the approach was to use RNAseq analysis to identify genes expressed in Xenopus epicardium that were affected by embryonic depletion of the epicardial transcription factor Tcf21 compared to control-MO injected siblings. Both upregulated and downregulated genes were validated by RT-PCR and whole embryo in situ hybridization to validate gene expression and assess spatio-temporal distribution of genes of interest within the heart and epicardium. Approximately 70-100 stage 44-46 Xenopus laevis hearts were dissected to isolate total mRNA from which poly-adenylated RNA was extracted using the Illumina standard protocol. This experiment represents one replicate from pooled hearts. mRNA profiles of stage 44-45 Xenopus laevis sibling hearts from control or Tcf21-depleted embryos, were generated by deep sequencing using Illumina GAII.
2013-07-05 | E-GEOD-45786 | biostudies-arrayexpress
Project description:Transcription factor 21 (TCF21) directly binds and regulates SF1 in tumor and normal adrenocortical cells, and both are involved in the development and steroidogenesis of the adrenal cortex. TCF21 is a tumor suppressor gene and its expression is reduced in malignant tumors. In adrenocortical tumors, it is less expressed in adrenocortical carcinomas (ACC) than in adrenocortical adenomas (ACA) and normal tissue. However, a comprehensive analysis to identify TCF21 targets have not yet been conducted in any type of cancer. In this study, we performed Chromatin Immunoprecipitation and Sequencing (ChIP-Seq) in adrenocortical carcinoma cell line (NCI-H295R) overexpressing TCF21, with the aim of identifying TCF21 new targets. The five most frequently identified sequences corresponded to the PRDM7, CNTNAP2, CACNA1B, PTPRN2 and KCNE1B genes. Validation experiments showed that, in NCI-H295R cells, TCF21 regulates gene expression positively in PRDM7 and negatively in CACNA1B. Recently, it was observed that the N-type calcium channel v2.2 (Cav2.2) encoded by CACNA1B gene is important in Angiotensin II signal transduction for corticosteroid biosynthesis in NCI-H295R adrenocortical carcinoma cells. Indeed, TCF21 inhibits CACNA1B and Cav2.2 expression in NCI-H295R. In addition, in a cohort of 55 adult patients with adrenocortical tumor, CACNA1B expression was higher in ACC than ACA, and was related to poor disease-free survival in ACC patients. These results suggest a mechanism of steroidogenesis control by TCF21 in adrenocortical tumor cells, in addition to the control observed through SF1 inhibition. Importantly, steroid production could impair tumor immunogenicity, contributing to the immune resistance described in adrenal cancer.
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