Fig 1: The cardiac fibroblast (CF) secretome increases neonatal rat ventricular myocyte (NRVM) size. A, Schematic of conditioned medium (CM) treatment of NRVMs (48 hours treatment with conditioned media from CFs). B, Coulter counter measurements of NRVMs treated for 48 hours with CM from CFs with or without 3 μmol/L SD208 to inhibit effects caused by TGFβ1 (transforming growth factor β 1) (N=CM from 3 CF isolations, 4 rats pooled per isolation, error bars show mean and SEM, 1‐way ANOVA, *P≤0.05, **P≤0.01). C, Coulter counter measurements of NRVM volume when treated with different concentrations of osteopontin (OPN), insulin growth factor 1 (IGF‐1), or phenylephrine (PE) (10 μmol/L), (N=2 isolations of NRVMs, N=3 for controls [same controls used for OPN and IGF‐1 treatment], error bars show SD, 1‐way ANOVA, significance compared with untreated, *P≤0.05, **P≤0.01). D, Schematic of CF signaling to NRVMs to induce hypertrophy through IGF‐1 signaling.
Fig 2: Schematic of TGFβ (transforming growth factor β) signaling and signaling through extracellular matrix (ECM) interactions to influence cytokine secretion.Cytokines that changed with TGFβ signaling vs ECM stiffness sensing are listed, and insulin growth factor 1 (IGF‐1), secreted by TGFβ‐activated myofibroblasts, caused hypertrophy. GM‐CSF indicates granulocyte‐macrophage colony‐stimulating factor; IGFBP, insulin growth factor binding protein; OPN, osteopontin; OPG, osteoprotegerin; WISP‐1, Wnt1 inducible signaling pathway protein 1; and CCL, Chemokine (C‐C motif) ligand.
Supplier Page from R&D Systems, a Bio-Techne Brand for Recombinant Rat IGF-I/IGF-1 Protein, CF