Table 1.
Disease Model | Methods of Fibroblast Identification | Sequencing Information | Number of Fibroblast Clusters/Activated Clusters | Primary Conclusions |
---|---|---|---|---|
Hypertension (ANG II, mouse) (18) | Differential gene expression (PDGFRa, Col1) | 10× chromium v2 kit, 12,000 cells (7,474 read from 2 hearts), Illumina Hiseq, 100,000 read/cell | 9/Fibro-Wif1, Fibro-Cilp, Fibro-Thbs4 | Two unique clusters: Fibro-Cilp and Fibro-Thbs4, identified after ANG II; Meox1: transcriptional switch for activation |
Hypertension (ANG II/PE, mouse) (88) | FACS-sorted PDGFRa+ cells as FAP+ and FAP− cells | 10× chromium v3.1 kit, Illumina NovasEq. 6,000, 100,000 reads/cell | 10/Postn/Fap cluster, Cxcl1 cluster, Acta2/Tagln cluster | Activated fibroblast cluster identified with higher Postn/Fap expression; IL-1β monoclonal antibody treatment ↓ FAP+ fibroblasts |
Hypertension (SHR) (17) | Col1a1+CD45−CD68−CD31− | 10× chromium v3 kit, (≈2,000 cells/sample read), 1 LV per sample, n = 7 per group, Illumina Hiseq4000 | 9/Proinflammatory (Ccl7, Ccl2), moderately fibrogenic (Ccn3), homeostatic, gateway | Transient ACE inhibition: ↑ proportion of cells in homeostatic cluster and ↓ proportion in gateway cluster |
Transverse aortic constriction (mouse) (89) | Differential gene expression | 10× chromium, 35,551 total cells read (13,937 fibroblasts) | 9/POSTN/FAP cluster | Fibroblasts shifted toward sham-like phenotype after JQ1 treatment |
Heart failure (human) (88) | Differential gene expression/cellular indexing of transcriptomes and epitopes (CITE) proteomics | 10× chromium v3.1 kit/ TotalseqA, 143,804 cells, Illumina NovasEq. 6,000 S4,104 read/cell | 13/POSTN/FAP cluster, CCL2/THBS1 cluster, ACTA2/TAGLN cluster | Postn/FAP cluster: major fibrogenic cluster in heart failure samples; CCL2 cluster: proinflammatory; Runx1 was major transcription factor for fibrosis |
ACE, angiotensin-converting enzyme; LV, left ventricle; SHR, spontaneously hypertensive rat.