Inhibiting Fibronectin Attenuates Fibrosis and Improves Cardiac Function in a Model of Heart Failure
BACKGROUND:Fibronectin (FN) polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblasts (MFs) after cardiac injury. We hypothesized that interfering with FN polymerization or its genetic ablation in fibroblasts would attenuate...
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| Published in | Circulation (New York, N.Y.) Vol. 138; no. 12; pp. 1236 - 1252 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
by the American College of Cardiology Foundation and the American Heart Association, Inc
18.09.2018
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | BACKGROUND:Fibronectin (FN) polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblasts (MFs) after cardiac injury. We hypothesized that interfering with FN polymerization or its genetic ablation in fibroblasts would attenuate MF and fibrosis and improve cardiac function after ischemia/reperfusion (I/R) injury.
METHODS:Mouse and human MFs were used to assess the impact of the FN polymerization inhibitor (pUR4) in attenuating pathological cellular features such as proliferation, migration, extracellular matrix deposition, and associated mechanisms. To evaluate the therapeutic potential of inhibiting FN polymerization in vivo, wild-type mice received daily intraperitoneal injections of either pUR4 or control peptide (III-11C) immediately after cardiac surgery for 7 consecutive days. Mice were analyzed 7 days after I/R to assess MF markers and inflammatory cell infiltration or 4 weeks after I/R to evaluate long-term effects of FN inhibition on cardiac function and fibrosis. Furthermore, inducible, fibroblast-restricted, FN gene–ablated (Tcf21;Fn) mice were used to evaluate cell specificity of FN expression and polymerization in the heart.
RESULTS:pUR4 administration on activated MFs reduced FN and collagen deposition into the extracellular matrix and attenuated cell proliferation, likely mediated through decreased c-myc signaling. pUR4 also ameliorated fibroblast migration accompanied by increased β1 integrin internalization and reduced levels of phosphorylated focal adhesion kinase protein. In vivo, daily administration of pUR4 for 7 days after I/R significantly reduced MF markers and neutrophil infiltration. This treatment regimen also significantly attenuated myocardial dysfunction, pathological cardiac remodeling, and fibrosis up to 4 weeks after I/R. Last, inducible ablation of FN in fibroblasts after I/R resulted in significant functional cardioprotection with reduced hypertrophy and fibrosis. The addition of pUR4 to the FN-ablated mice did not confer further cardioprotection, suggesting that the salutary effects of inhibiting FN polymerization may be mediated largely through effects on FN secreted from the cardiac fibroblast lineage.
CONCLUSIONS:Inhibiting FN polymerization or cardiac fibroblast gene expression attenuates pathological properties of MFs in vitro and ameliorates adverse cardiac remodeling and fibrosis in an in vivo model of heart failure. Interfering with FN polymerization may be a new therapeutic strategy for treating cardiac fibrosis and heart failure. |
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| AbstractList | Background:
Fibronectin (FN) polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblasts (MFs) after cardiac injury. We hypothesized that interfering with FN polymerization or its genetic ablation in fibroblasts would attenuate MF and fibrosis and improve cardiac function after ischemia/reperfusion (I/R) injury.
Methods:
Mouse and human MFs were used to assess the impact of the FN polymerization inhibitor (pUR4) in attenuating pathological cellular features such as proliferation, migration, extracellular matrix deposition, and associated mechanisms. To evaluate the therapeutic potential of inhibiting FN polymerization in vivo, wild-type mice received daily intraperitoneal injections of either pUR4 or control peptide (III-11C) immediately after cardiac surgery for 7 consecutive days. Mice were analyzed 7 days after I/R to assess MF markers and inflammatory cell infiltration or 4 weeks after I/R to evaluate long-term effects of FN inhibition on cardiac function and fibrosis. Furthermore, inducible, fibroblast-restricted, FN gene–ablated (Tcf21
MerCreMer
;
Fn
flox
) mice were used to evaluate cell specificity of FN expression and polymerization in the heart.
Results:
pUR4 administration on activated MFs reduced FN and collagen deposition into the extracellular matrix and attenuated cell proliferation, likely mediated through decreased c-myc signaling. pUR4 also ameliorated fibroblast migration accompanied by increased β1 integrin internalization and reduced levels of phosphorylated focal adhesion kinase protein. In vivo, daily administration of pUR4 for 7 days after I/R significantly reduced MF markers and neutrophil infiltration. This treatment regimen also significantly attenuated myocardial dysfunction, pathological cardiac remodeling, and fibrosis up to 4 weeks after I/R. Last, inducible ablation of FN in fibroblasts after I/R resulted in significant functional cardioprotection with reduced hypertrophy and fibrosis. The addition of pUR4 to the FN-ablated mice did not confer further cardioprotection, suggesting that the salutary effects of inhibiting FN polymerization may be mediated largely through effects on FN secreted from the cardiac fibroblast lineage.
Conclusions:
Inhibiting FN polymerization or cardiac fibroblast gene expression attenuates pathological properties of MFs in vitro and ameliorates adverse cardiac remodeling and fibrosis in an in vivo model of heart failure. Interfering with FN polymerization may be a new therapeutic strategy for treating cardiac fibrosis and heart failure. BACKGROUND—Fibronectin (FN) polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblasts (MF) following cardiac injury. We hypothesized that interfering with FN polymerization or its genetic ablation in fibroblasts would attenuate MF, fibrosis and improve cardiac function following ischemia/reperfusion (I/R)-injury. METHODS—Mouse and human MF were utilized to assess the impact of the FN polymerization inhibitor (pUR4) in attenuating pathologic cellular features such as proliferation, migration, extracellular matrix (ECM) deposition and associated mechanisms. To evaluate the therapeutic potential of inhibiting FN polymerization in vivo, wildtype (WT) mice received daily intraperitoneal injections of either pUR4 or control peptide (III-11C) immediately after cardiac surgery, for seven consecutive days. Mice were analyzed seven days post-I/R to assess myofibroblast markers and inflammatory cell infiltration, or four weeks post-I/R, to evaluate long-term effects of FN inhibition on cardiac function and fibrosis. Further, inducible, fibroblast-restricted, FN gene ablated (Tcf21;Fn) mice were utilized to evaluate cell specificity of FN expression and polymerization in the heart. RESULTS—pUR4 administration on activated MF reduced FN and collagen deposition into the ECM and attenuated cell proliferation, likely mediated through decreased c-myc signaling. pUR4 also ameliorated fibroblast migration accompanied by increased β1 integrin internalization and reduced levels of phosphorylated focal adhesion kinase (FAK) protein. In vivo, daily administration of pUR4 for seven days post-I/R significantly reduced MF markers and neutrophil infiltration. This treatment regimen also significantly attenuated myocardial dysfunction, pathologic cardiac remodeling and fibrosis up to 4 weeks post-I/R. Finally, inducible ablation of FN in fibroblasts post-I/R resulted in significant functional cardioprotection with reduced hypertrophy and fibrosis. Interestingly, addition of pUR4 to the FN ablated mice did not confer further cardioprotection, suggesting that the salutary effects of inhibiting FN polymerization may be largely mediated through effects on FN secreted from the CF lineage. CONCLUSIONS—Inhibiting FN polymerization or CF gene expression attenuates pathologic properties of MF in vitro and ameliorates adverse cardiac remodeling and fibrosis in an in vivo model of HF. Interfering with FN polymerization may be a new therapeutic strategy for treating cardiac fibrosis and HF. Fibronectin (FN) polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblasts (MFs) after cardiac injury. We hypothesized that interfering with FN polymerization or its genetic ablation in fibroblasts would attenuate MF and fibrosis and improve cardiac function after ischemia/reperfusion (I/R) injury. Mouse and human MFs were used to assess the impact of the FN polymerization inhibitor (pUR4) in attenuating pathological cellular features such as proliferation, migration, extracellular matrix deposition, and associated mechanisms. To evaluate the therapeutic potential of inhibiting FN polymerization in vivo, wild-type mice received daily intraperitoneal injections of either pUR4 or control peptide (III-11C) immediately after cardiac surgery for 7 consecutive days. Mice were analyzed 7 days after I/R to assess MF markers and inflammatory cell infiltration or 4 weeks after I/R to evaluate long-term effects of FN inhibition on cardiac function and fibrosis. Furthermore, inducible, fibroblast-restricted, FN gene-ablated (Tcf21 ; Fn ) mice were used to evaluate cell specificity of FN expression and polymerization in the heart. pUR4 administration on activated MFs reduced FN and collagen deposition into the extracellular matrix and attenuated cell proliferation, likely mediated through decreased c-myc signaling. pUR4 also ameliorated fibroblast migration accompanied by increased β1 integrin internalization and reduced levels of phosphorylated focal adhesion kinase protein. In vivo, daily administration of pUR4 for 7 days after I/R significantly reduced MF markers and neutrophil infiltration. This treatment regimen also significantly attenuated myocardial dysfunction, pathological cardiac remodeling, and fibrosis up to 4 weeks after I/R. Last, inducible ablation of FN in fibroblasts after I/R resulted in significant functional cardioprotection with reduced hypertrophy and fibrosis. The addition of pUR4 to the FN-ablated mice did not confer further cardioprotection, suggesting that the salutary effects of inhibiting FN polymerization may be mediated largely through effects on FN secreted from the cardiac fibroblast lineage. Inhibiting FN polymerization or cardiac fibroblast gene expression attenuates pathological properties of MFs in vitro and ameliorates adverse cardiac remodeling and fibrosis in an in vivo model of heart failure. Interfering with FN polymerization may be a new therapeutic strategy for treating cardiac fibrosis and heart failure. BACKGROUNDFibronectin (FN) polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblasts (MFs) after cardiac injury. We hypothesized that interfering with FN polymerization or its genetic ablation in fibroblasts would attenuate MF and fibrosis and improve cardiac function after ischemia/reperfusion (I/R) injury.METHODSMouse and human MFs were used to assess the impact of the FN polymerization inhibitor (pUR4) in attenuating pathological cellular features such as proliferation, migration, extracellular matrix deposition, and associated mechanisms. To evaluate the therapeutic potential of inhibiting FN polymerization in vivo, wild-type mice received daily intraperitoneal injections of either pUR4 or control peptide (III-11C) immediately after cardiac surgery for 7 consecutive days. Mice were analyzed 7 days after I/R to assess MF markers and inflammatory cell infiltration or 4 weeks after I/R to evaluate long-term effects of FN inhibition on cardiac function and fibrosis. Furthermore, inducible, fibroblast-restricted, FN gene-ablated (Tcf21MerCreMer; Fnflox) mice were used to evaluate cell specificity of FN expression and polymerization in the heart.RESULTSpUR4 administration on activated MFs reduced FN and collagen deposition into the extracellular matrix and attenuated cell proliferation, likely mediated through decreased c-myc signaling. pUR4 also ameliorated fibroblast migration accompanied by increased β1 integrin internalization and reduced levels of phosphorylated focal adhesion kinase protein. In vivo, daily administration of pUR4 for 7 days after I/R significantly reduced MF markers and neutrophil infiltration. This treatment regimen also significantly attenuated myocardial dysfunction, pathological cardiac remodeling, and fibrosis up to 4 weeks after I/R. Last, inducible ablation of FN in fibroblasts after I/R resulted in significant functional cardioprotection with reduced hypertrophy and fibrosis. The addition of pUR4 to the FN-ablated mice did not confer further cardioprotection, suggesting that the salutary effects of inhibiting FN polymerization may be mediated largely through effects on FN secreted from the cardiac fibroblast lineage.CONCLUSIONSInhibiting FN polymerization or cardiac fibroblast gene expression attenuates pathological properties of MFs in vitro and ameliorates adverse cardiac remodeling and fibrosis in an in vivo model of heart failure. Interfering with FN polymerization may be a new therapeutic strategy for treating cardiac fibrosis and heart failure. BACKGROUND:Fibronectin (FN) polymerization is necessary for collagen matrix deposition and is a key contributor to increased abundance of cardiac myofibroblasts (MFs) after cardiac injury. We hypothesized that interfering with FN polymerization or its genetic ablation in fibroblasts would attenuate MF and fibrosis and improve cardiac function after ischemia/reperfusion (I/R) injury. METHODS:Mouse and human MFs were used to assess the impact of the FN polymerization inhibitor (pUR4) in attenuating pathological cellular features such as proliferation, migration, extracellular matrix deposition, and associated mechanisms. To evaluate the therapeutic potential of inhibiting FN polymerization in vivo, wild-type mice received daily intraperitoneal injections of either pUR4 or control peptide (III-11C) immediately after cardiac surgery for 7 consecutive days. Mice were analyzed 7 days after I/R to assess MF markers and inflammatory cell infiltration or 4 weeks after I/R to evaluate long-term effects of FN inhibition on cardiac function and fibrosis. Furthermore, inducible, fibroblast-restricted, FN gene–ablated (Tcf21;Fn) mice were used to evaluate cell specificity of FN expression and polymerization in the heart. RESULTS:pUR4 administration on activated MFs reduced FN and collagen deposition into the extracellular matrix and attenuated cell proliferation, likely mediated through decreased c-myc signaling. pUR4 also ameliorated fibroblast migration accompanied by increased β1 integrin internalization and reduced levels of phosphorylated focal adhesion kinase protein. In vivo, daily administration of pUR4 for 7 days after I/R significantly reduced MF markers and neutrophil infiltration. This treatment regimen also significantly attenuated myocardial dysfunction, pathological cardiac remodeling, and fibrosis up to 4 weeks after I/R. Last, inducible ablation of FN in fibroblasts after I/R resulted in significant functional cardioprotection with reduced hypertrophy and fibrosis. The addition of pUR4 to the FN-ablated mice did not confer further cardioprotection, suggesting that the salutary effects of inhibiting FN polymerization may be mediated largely through effects on FN secreted from the cardiac fibroblast lineage. CONCLUSIONS:Inhibiting FN polymerization or cardiac fibroblast gene expression attenuates pathological properties of MFs in vitro and ameliorates adverse cardiac remodeling and fibrosis in an in vivo model of heart failure. Interfering with FN polymerization may be a new therapeutic strategy for treating cardiac fibrosis and heart failure. |
| Author | Potter, Sarah J Gibson, Aaron M Alcaide, Pilar Salvador, Ane M Sargent, Michelle A Perkins, Charles Valiente-Alandi, Iñigo Carrillo-Salinas, Francisco Schafer, Allison E DeFalco, Tony Schips, Tobias Huo, Jiuzhou Lorenz, John N Molkentin, Jeffery D Nieman, Michelle L Blaxall, Burns C |
| AuthorAffiliation | Department of Pediatrics (I.V.-A., A.E.S., T.S., A.M.G., C.P., M.A.S., J.H., J.D.M., B.C.B.), University of Cincinnati College of Medicine, OH. Department of Molecular and Cellular Physiology (M.C.N., J.N.L., University of Cincinnati College of Medicine, OH. Ohio Heart Institute (I.V.-A., A.E.S., T.S., A.M.G., C.P., M.A.S., J.H., J.D.M., B.C.B.), Cincinnati Children’s Hospital Medical Center. Division of Reproductive Sciences (S.J.P., T.D.), Cincinnati Children’s Hospital Medical Center. Department of Integrative Physiology and Pathobiology, Tufts University Schools of Medicine, Boston, MA (A.M.S., F.C.-S., P.A.) |
| AuthorAffiliation_xml | – name: Department of Pediatrics (I.V.-A., A.E.S., T.S., A.M.G., C.P., M.A.S., J.H., J.D.M., B.C.B.), University of Cincinnati College of Medicine, OH. Department of Molecular and Cellular Physiology (M.C.N., J.N.L., University of Cincinnati College of Medicine, OH. Ohio Heart Institute (I.V.-A., A.E.S., T.S., A.M.G., C.P., M.A.S., J.H., J.D.M., B.C.B.), Cincinnati Children’s Hospital Medical Center. Division of Reproductive Sciences (S.J.P., T.D.), Cincinnati Children’s Hospital Medical Center. Department of Integrative Physiology and Pathobiology, Tufts University Schools of Medicine, Boston, MA (A.M.S., F.C.-S., P.A.) – name: Department of Integrative Physiology and Pathobiology, Tufts University Schools of Medicine, Boston, MA – name: Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati OH – name: Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH & Heart Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH – name: Division of Reproductive Sciences, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH – name: 3 Department of Integrative Physiology and Pathobiology, Tufts University Schools of Medicine, Boston, MA – name: 2 Division of Reproductive Sciences, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH – name: 1 Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH Heart Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH – name: 4 Department of Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati OH |
| Author_xml | – sequence: 1 givenname: Iñigo surname: Valiente-Alandi fullname: Valiente-Alandi, Iñigo organization: Department of Pediatrics (I.V.-A., A.E.S., T.S., A.M.G., C.P., M.A.S., J.H., J.D.M., B.C.B.), University of Cincinnati College of Medicine, OH. Department of Molecular and Cellular Physiology (M.C.N., J.N.L., University of Cincinnati College of Medicine, OH. Ohio Heart Institute (I.V.-A., A.E.S., T.S., A.M.G., C.P., M.A.S., J.H., J.D.M., B.C.B.), Cincinnati Children’s Hospital Medical Center. Division of Reproductive Sciences (S.J.P., T.D.), Cincinnati Children’s Hospital Medical Center. Department of Integrative Physiology and Pathobiology, Tufts University Schools of Medicine, Boston, MA (A.M.S., F.C.-S., P.A.) – sequence: 2 givenname: Sarah surname: Potter middlename: J fullname: Potter, Sarah J – sequence: 3 givenname: Ane surname: Salvador middlename: M fullname: Salvador, Ane M – sequence: 4 givenname: Allison surname: Schafer middlename: E fullname: Schafer, Allison E – sequence: 5 givenname: Tobias surname: Schips fullname: Schips, Tobias – sequence: 6 givenname: Francisco surname: Carrillo-Salinas fullname: Carrillo-Salinas, Francisco – sequence: 7 givenname: Aaron surname: Gibson middlename: M fullname: Gibson, Aaron M – sequence: 8 givenname: Michelle surname: Nieman middlename: L fullname: Nieman, Michelle L – sequence: 9 givenname: Charles surname: Perkins fullname: Perkins, Charles – sequence: 10 givenname: Michelle surname: Sargent middlename: A fullname: Sargent, Michelle A – sequence: 11 givenname: Jiuzhou surname: Huo fullname: Huo, Jiuzhou – sequence: 12 givenname: John surname: Lorenz middlename: N fullname: Lorenz, John N – sequence: 13 givenname: Tony surname: DeFalco fullname: DeFalco, Tony – sequence: 14 givenname: Jeffery surname: Molkentin middlename: D fullname: Molkentin, Jeffery D – sequence: 15 givenname: Pilar surname: Alcaide fullname: Alcaide, Pilar – sequence: 16 givenname: Burns surname: Blaxall middlename: C fullname: Blaxall, Burns C |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29653926$$D View this record in MEDLINE/PubMed |
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