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Autocrine Sfrp1 inhibits fibroblast invasion during transition to injury induced myofibroblasts - Tcf21 labeled mice

ABSTRACT: Autocrine Sfrp1 inhibits fibroblast invasion during transition to injury induced myofibroblasts - Tcf21 labeled mice

PROVIDER: PRJNA856687 | ENA |

REPOSITORIES: ENA

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			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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Autocrine Sfrp1 inhibits fibroblast invasion during transition to injury induced myofibroblasts - Tcf21 labeled mice

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

Autocrine Sfrp1 inhibits lung fibroblast invasion during transition to injury induced myofibroblasts

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

Autocrine Sfrp1 inhibits fibroblast invasion during transition to injury induced myofibroblasts - daily profiling of mouse lungs after Bleomycin injury

2022-10-12 | GSE207851 | GEO

Autocrine Sfrp1 inhibits lung fibroblast invasion during transition to injury induced myofibroblasts

Project description:Autocrine Sfrp1 inhibits lung fibroblast invasion during transition to injury induced myofibroblasts

| PRJNA856233 | ENA

Autocrine Sfrp1 inhibits fibroblast invasion during transition to injury induced myofibroblasts - daily profiling of mouse lungs after Bleomycin injury

Project description:Autocrine Sfrp1 inhibits fibroblast invasion during transition to injury induced myofibroblasts - daily profiling of mouse lungs after Bleomycin injury

| PRJNA857439 | ENA

Cancer-derived myofibroblasts vs. non-cancer derived myofibroblasts

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

Down-regulation of SFRP1 in a mammary epithelial cell line

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

Secretomes of Cancer-Associated Myofibroblasts and Normal Tissue Myofibroblasts in hypoxia and normoxia C4PR_LIV

Project description:Cancer-associated fibroblasts are a major component of the cancer stroma. Here we focus on gastric cancer associated myofibroblasts (CAMs). CAMs secrete factors that increase the migration, invasion and proliferation of cancer cells when compared to adjacent tissue myofibroblasts (ATMs), or normal tissue myofibroblasts (NTMs). In this study we identified and quantified the proteins secreted by normoxic (21% O2) and hypoxic (1% O2) myofibroblast cells.

2019-03-04 | PXD008104 | Pride

Genetic lineage tracing defines myofibroblast origin and function in the injured heart

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

2016-06-14 | E-GEOD-83337 | biostudies-arrayexpress

Cardiac transcriptome of Tcf21-depleted Xenopus embryos

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

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