Summary of Study ST002805

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench,, where it has been assigned Project ID PR001752. The data can be accessed directly via it's Project DOI: 10.21228/M87Q7Z This work is supported by NIH grant, U2C- DK119886.


This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

Perform statistical analysis  |  Show all samples  |  Show named metabolites  |  Download named metabolite data  
Download mwTab file (text)   |  Download mwTab file(JSON)   |  Download data files (Contains raw data)
Study IDST002805
Study TitleIL-1β-mediated adaptive re-programming of endogenous human cardiac fibroblasts to cells with immune features during fibrotic remodeling
Study SummaryThe source and roles of fibroblasts and CD4 helper T-cells during maladaptive remodeling and myocardial fibrosis in pulmonary arterial hypertension (PAH) have been long debated. We demonstrate, using single-cell mass cytometry, a sub-population of endogenous human cardiac fibroblasts expressing increased levels of CD4, a helper T-cell marker, in addition to myofibroblast markers distributed in human fibrotic RV tissue, interstitial/perivascular lesions of SUGEN/Hypoxia (SuHx) rats and fibroblasts labelled with pdgfrα CreERt2/+ in R26R-tdTomato mice. Recombinant IL-1β increases IL-1R, CCR2 receptor expression, modifies the secretome, and differentiates cardiac fibroblasts to form CD68 positive cell clusters. IL-1β also activates stemness markers such as NANOG and SOX2 and genes involved in de-differentiation, lymphoid cell function and metabolic reprogramming. IL-1β induction of lineage traced primary mouse cardiac fibroblasts causes these cells to lose their fibroblast identity and acquire an immune phenotype. Our results identify IL-1β induced immune-competency in human cardiac fibroblasts and suggest that fibroblast secretome modulation may constitute a therapeutic approach to PAH and other diseases typified by inflammation and fibrotic remodeling.
Brown University
DepartmentMolecular Pharmacology, Physiology and Biotechnology
LaboratorySiamwala Lab
Last NameSiamwala
First NameJamila
Address830 Chalkstone Avenue, Building 35
Submit Date2023-07-18
Raw Data AvailableYes
Raw Data File Type(s)wiff
Analysis Type DetailOther
Release Date2023-08-07
Release Version1
Jamila Siamwala Jamila Siamwala application/zip

Select appropriate tab below to view additional metadata details:


Subject type: Cultured cells; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Sex Treatment
SA300847534282_cF Control
SA300848534282_tF IL-1B
SA3008491281202_cM Control
SA30085062122_cM Control
SA30085162122_tM IL-1B
SA3008521281202_tM IL-1B
Showing results 1 to 6 of 6