Combined genetic-pharmacologic inactivation of tightly linked ADAMTS proteases in temporally specific windows uncovers distinct roles for versican proteolysis and glypican-6 in cardiac development
• Combined genetic-pharmacologic ADAMTS1 and ADAMTS5 inactivation in mice.• Degradomics identification of putative ADAMTS1 and ADAMTS5 substrates.• A requirement for versican proteolysis and glypican-6 in heart development.• Novel roles for ADAMTS1, ADAMTS5 and glypican-6 in hedgehog signaling in th...
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| Published in | Matrix biology Vol. 131; pp. 1 - 16 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Netherlands
Elsevier B.V
01.08.2024
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| Abstract | • Combined genetic-pharmacologic ADAMTS1 and ADAMTS5 inactivation in mice.• Degradomics identification of putative ADAMTS1 and ADAMTS5 substrates.• A requirement for versican proteolysis and glypican-6 in heart development.• Novel roles for ADAMTS1, ADAMTS5 and glypican-6 in hedgehog signaling in the heart.
Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases ADAMTS1 and ADAMTS5, are extensively co-expressed during mouse cardiac development. The mouse mutants of each gene have mild cardiac anomalies, however, their combined genetic inactivation to elicit cooperative roles is precluded by tight gene linkage. Therefore, we coupled Adamts1 inactivation with pharmacologic ADAMTS5 blockade to uncover stage-specific cooperative roles and investigated their potential substrates in mouse cardiac development. ADAMTS5 blockade was achieved in Adamts1 null mouse embryos using an activity-blocking monoclonal antibody during distinct developmental windows spanning myocardial compaction or cardiac septation and outflow tract rotation. Synchrotron imaging, RNA in situ hybridization, immunofluorescence microscopy and electron microscopy were used to determine the impact on cardiac development and compared to Gpc6 and ADAMTS-cleavage resistant versican mutants. Mass spectrometry-based N-terminomics was used to seek relevant substrates. Combined inactivation of ADAMTS1 and ADAMTS5 prior to 12.5 days of gestation led to dramatic accumulation of versican-rich cardiac jelly and inhibited formation of compact and trabecular myocardium, which was also observed in mice with ADAMTS cleavage-resistant versican. Combined inactivation after 12.5 days impaired outflow tract development and ventricular septal closure, generating a tetralogy of Fallot-like defect. N-terminomics of combined ADAMTS knockout and control hearts identified a cleaved glypican-6 peptide only in the controls. ADAMTS1 and ADAMTS5 expression in cells was associated with specific glypican-6 cleavages. Paradoxically, combined ADAMTS1 and ADAMTS5 inactivation reduced cardiac glypican-6 and outflow tract Gpc6 transcription. Notably, Gpc6−/− hearts demonstrated similar rotational defects as combined ADAMTS inactivated hearts and both had reduced hedgehog signaling. Thus, versican proteolysis in cardiac jelly at the canonical Glu441-Ala442 site is cooperatively mediated by ADAMTS1 and ADAMTS5 and required for proper ventricular cardiomyogenesis, whereas, reduced glypican-6 after combined ADAMTS inactivation impairs hedgehog signaling, leading to outflow tract malrotation. |
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| AbstractList | Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases ADAMTS1 and ADAMTS5, are extensively co-expressed during mouse cardiac development. The mouse mutants of each gene have mild cardiac anomalies, however, their combined genetic inactivation to elicit cooperative roles is precluded by tight gene linkage. Therefore, we coupled Adamts1 inactivation with pharmacologic ADAMTS5 blockade to uncover stage-specific cooperative roles and investigated their potential substrates in mouse cardiac development. ADAMTS5 blockade was achieved in Adamts1 null mouse embryos using an activity-blocking monoclonal antibody during distinct developmental windows spanning myocardial compaction or cardiac septation and outflow tract rotation. Synchrotron imaging, RNA in situ hybridization, immunofluorescence microscopy and electron microscopy were used to determine the impact on cardiac development and compared to Gpc6 and ADAMTS-cleavage resistant versican mutants. Mass spectrometry-based N-terminomics was used to seek relevant substrates. Combined inactivation of ADAMTS1 and ADAMTS5 prior to 12.5 days of gestation led to dramatic accumulation of versican-rich cardiac jelly and inhibited formation of compact and trabecular myocardium, which was also observed in mice with ADAMTS cleavage-resistant versican. Combined inactivation after 12.5 days impaired outflow tract development and ventricular septal closure, generating a tetralogy of Fallot-like defect. N-terminomics of combined ADAMTS knockout and control hearts identified a cleaved glypican-6 peptide only in the controls. ADAMTS1 and ADAMTS5 expression in cells was associated with specific glypican-6 cleavages. Paradoxically, combined ADAMTS1 and ADAMTS5 inactivation reduced cardiac glypican-6 and outflow tract Gpc6 transcription. Notably, Gpc6−/− hearts demonstrated similar rotational defects as combined ADAMTS inactivated hearts and both had reduced hedgehog signaling. Thus, versican proteolysis in cardiac jelly at the canonical Glu441-Ala442 site is cooperatively mediated by ADAMTS1 and ADAMTS5 and required for proper ventricular cardiomyogenesis, whereas, reduced glypican-6 after combined ADAMTS inactivation impairs hedgehog signaling, leading to outflow tract malrotation. Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases ADAMTS1 and ADAMTS5, are extensively co-expressed during mouse cardiac development. The mouse mutants of each gene have mild cardiac anomalies, however, their combined genetic inactivation to elicit cooperative roles is precluded by tight gene linkage. Therefore, we coupled Adamts1 inactivation with pharmacologic ADAMTS5 blockade to uncover stage-specific cooperative roles and investigated their potential substrates in mouse cardiac development. ADAMTS5 blockade was achieved in Adamts1 null mouse embryos using an activity-blocking monoclonal antibody during distinct developmental windows spanning myocardial compaction or cardiac septation and outflow tract rotation. Synchrotron imaging, RNA in situ hybridization, immunofluorescence microscopy and electron microscopy were used to determine the impact on cardiac development and compared to Gpc6 and ADAMTS-cleavage resistant versican mutants. Mass spectrometry-based N-terminomics was used to seek relevant substrates. Combined inactivation of ADAMTS1 and ADAMTS5 prior to 12.5 days of gestation led to dramatic accumulation of versican-rich cardiac jelly and inhibited formation of compact and trabecular myocardium, which was also observed in mice with ADAMTS cleavage-resistant versican. Combined inactivation after 12.5 days impaired outflow tract development and ventricular septal closure, generating a tetralogy of Fallot-like defect. N-terminomics of combined ADAMTS knockout and control hearts identified a cleaved glypican-6 peptide only in the controls. ADAMTS1 and ADAMTS5 expression in cells was associated with specific glypican-6 cleavages. Paradoxically, combined ADAMTS1 and ADAMTS5 inactivation reduced cardiac glypican-6 and outflow tract Gpc6 transcription. Notably, Gpc6-/- hearts demonstrated similar rotational defects as combined ADAMTS inactivated hearts and both had reduced hedgehog signaling. Thus, versican proteolysis in cardiac jelly at the canonical Glu441-Ala442 site is cooperatively mediated by ADAMTS1 and ADAMTS5 and required for proper ventricular cardiomyogenesis, whereas, reduced glypican-6 after combined ADAMTS inactivation impairs hedgehog signaling, leading to outflow tract malrotation.Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases ADAMTS1 and ADAMTS5, are extensively co-expressed during mouse cardiac development. The mouse mutants of each gene have mild cardiac anomalies, however, their combined genetic inactivation to elicit cooperative roles is precluded by tight gene linkage. Therefore, we coupled Adamts1 inactivation with pharmacologic ADAMTS5 blockade to uncover stage-specific cooperative roles and investigated their potential substrates in mouse cardiac development. ADAMTS5 blockade was achieved in Adamts1 null mouse embryos using an activity-blocking monoclonal antibody during distinct developmental windows spanning myocardial compaction or cardiac septation and outflow tract rotation. Synchrotron imaging, RNA in situ hybridization, immunofluorescence microscopy and electron microscopy were used to determine the impact on cardiac development and compared to Gpc6 and ADAMTS-cleavage resistant versican mutants. Mass spectrometry-based N-terminomics was used to seek relevant substrates. Combined inactivation of ADAMTS1 and ADAMTS5 prior to 12.5 days of gestation led to dramatic accumulation of versican-rich cardiac jelly and inhibited formation of compact and trabecular myocardium, which was also observed in mice with ADAMTS cleavage-resistant versican. Combined inactivation after 12.5 days impaired outflow tract development and ventricular septal closure, generating a tetralogy of Fallot-like defect. N-terminomics of combined ADAMTS knockout and control hearts identified a cleaved glypican-6 peptide only in the controls. ADAMTS1 and ADAMTS5 expression in cells was associated with specific glypican-6 cleavages. Paradoxically, combined ADAMTS1 and ADAMTS5 inactivation reduced cardiac glypican-6 and outflow tract Gpc6 transcription. Notably, Gpc6-/- hearts demonstrated similar rotational defects as combined ADAMTS inactivated hearts and both had reduced hedgehog signaling. Thus, versican proteolysis in cardiac jelly at the canonical Glu441-Ala442 site is cooperatively mediated by ADAMTS1 and ADAMTS5 and required for proper ventricular cardiomyogenesis, whereas, reduced glypican-6 after combined ADAMTS inactivation impairs hedgehog signaling, leading to outflow tract malrotation. Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases ADAMTS1 and ADAMTS5, are extensively co-expressed during mouse cardiac development. The mouse mutants of each gene have mild cardiac anomalies, however, their combined genetic inactivation to elicit cooperative roles is precluded by tight gene linkage. Therefore, we coupled Adamts1 inactivation with pharmacologic ADAMTS5 blockade to uncover stage-specific cooperative roles and investigated their potential substrates in mouse cardiac development. ADAMTS5 blockade was achieved in Adamts1 null mouse embryos using an activity-blocking monoclonal antibody during distinct developmental windows spanning myocardial compaction or cardiac septation and outflow tract rotation. Synchrotron imaging, RNA in situ hybridization, immunofluorescence microscopy and electron microscopy were used to determine the impact on cardiac development and compared to Gpc6 and ADAMTS-cleavage resistant versican mutants. Mass spectrometry-based N-terminomics was used to seek relevant substrates. Combined inactivation of ADAMTS1 and ADAMTS5 prior to 12.5 days of gestation led to dramatic accumulation of versican-rich cardiac jelly and inhibited formation of compact and trabecular myocardium, which was also observed in mice with ADAMTS cleavage-resistant versican. Combined inactivation after 12.5 days impaired outflow tract development and ventricular septal closure, generating a tetralogy of Fallot-like defect. N-terminomics of combined ADAMTS knockout and control hearts identified a cleaved glypican-6 peptide only in the controls. ADAMTS1 and ADAMTS5 expression in cells was associated with specific glypican-6 cleavages. Paradoxically, combined ADAMTS1 and ADAMTS5 inactivation reduced cardiac glypican-6 and outflow tract Gpc6 transcription. Notably, Gpc6 hearts demonstrated similar rotational defects as combined ADAMTS inactivated hearts and both had reduced hedgehog signaling. Thus, versican proteolysis in cardiac jelly at the canonical Glu -Ala site is cooperatively mediated by ADAMTS1 and ADAMTS5 and required for proper ventricular cardiomyogenesis, whereas, reduced glypican-6 after combined ADAMTS inactivation impairs hedgehog signaling, leading to outflow tract malrotation. Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases ADAMTS1 and ADAMTS5, are extensively co-expressed during mouse cardiac development. The mouse mutants of each gene have mild cardiac anomalies, however, their combined genetic inactivation to elicit cooperative roles is precluded by tight gene linkage. Therefore, we coupled Adamts1 inactivation with pharmacologic ADAMTS5 blockade to uncover stage-specific cooperative roles and investigated their potential substrates in mouse cardiac development. ADAMTS5 blockade was achieved in Adamts1 null mouse embryos using an activity-blocking monoclonal antibody during distinct developmental windows spanning myocardial compaction or cardiac septation and outflow tract rotation. Synchrotron imaging, RNA in situ hybridization, immunofluorescence microscopy and electron microscopy were used to determine the impact on cardiac development and compared to Gpc6 and ADAMTS-cleavage resistant versican mutants. Mass spectrometry-based N-terminomics was used to seek relevant substrates. Combined inactivation of ADAMTS1 and ADAMTS5 prior to 12.5 days of gestation led to dramatic accumulation of versican-rich cardiac jelly and inhibited formation of compact and trabecular myocardium, which was also observed in mice with ADAMTS cleavage-resistant versican. Combined inactivation after 12.5 days impaired outflow tract development and ventricular septal closure, generating a tetralogy of Fallot-like defect. N-terminomics of combined ADAMTS knockout and control hearts identified a cleaved glypican-6 peptide only in the controls. ADAMTS1 and ADAMTS5 expression in cells was associated with specific glypican-6 cleavages. Paradoxically, combined ADAMTS1 and ADAMTS5 inactivation reduced cardiac glypican-6 and outflow tract Gpc6 transcription. Notably, Gpc6 −/− hearts demonstrated similar rotational defects as combined ADAMTS inactivated hearts and both had reduced hedgehog signaling. Thus, versican proteolysis in cardiac jelly at the canonical Glu 441 -Ala 442 site is cooperatively mediated by ADAMTS1 and ADAMTS5 and required for proper ventricular cardiomyogenesis, whereas, reduced glypican-6 after combined ADAMTS inactivation impairs hedgehog signaling, leading to outflow tract malrotation. • Combined genetic-pharmacologic ADAMTS1 and ADAMTS5 inactivation in mice.• Degradomics identification of putative ADAMTS1 and ADAMTS5 substrates.• A requirement for versican proteolysis and glypican-6 in heart development.• Novel roles for ADAMTS1, ADAMTS5 and glypican-6 in hedgehog signaling in the heart. Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases ADAMTS1 and ADAMTS5, are extensively co-expressed during mouse cardiac development. The mouse mutants of each gene have mild cardiac anomalies, however, their combined genetic inactivation to elicit cooperative roles is precluded by tight gene linkage. Therefore, we coupled Adamts1 inactivation with pharmacologic ADAMTS5 blockade to uncover stage-specific cooperative roles and investigated their potential substrates in mouse cardiac development. ADAMTS5 blockade was achieved in Adamts1 null mouse embryos using an activity-blocking monoclonal antibody during distinct developmental windows spanning myocardial compaction or cardiac septation and outflow tract rotation. Synchrotron imaging, RNA in situ hybridization, immunofluorescence microscopy and electron microscopy were used to determine the impact on cardiac development and compared to Gpc6 and ADAMTS-cleavage resistant versican mutants. Mass spectrometry-based N-terminomics was used to seek relevant substrates. Combined inactivation of ADAMTS1 and ADAMTS5 prior to 12.5 days of gestation led to dramatic accumulation of versican-rich cardiac jelly and inhibited formation of compact and trabecular myocardium, which was also observed in mice with ADAMTS cleavage-resistant versican. Combined inactivation after 12.5 days impaired outflow tract development and ventricular septal closure, generating a tetralogy of Fallot-like defect. N-terminomics of combined ADAMTS knockout and control hearts identified a cleaved glypican-6 peptide only in the controls. ADAMTS1 and ADAMTS5 expression in cells was associated with specific glypican-6 cleavages. Paradoxically, combined ADAMTS1 and ADAMTS5 inactivation reduced cardiac glypican-6 and outflow tract Gpc6 transcription. Notably, Gpc6−/− hearts demonstrated similar rotational defects as combined ADAMTS inactivated hearts and both had reduced hedgehog signaling. Thus, versican proteolysis in cardiac jelly at the canonical Glu441-Ala442 site is cooperatively mediated by ADAMTS1 and ADAMTS5 and required for proper ventricular cardiomyogenesis, whereas, reduced glypican-6 after combined ADAMTS inactivation impairs hedgehog signaling, leading to outflow tract malrotation. |
| Author | Larkin, Jonathan Tran-Lundmark, Karin Filmus, Jorge Apte, Suneel S. Bhutada, Sumit Nelson, Courtney M. Seifert, Deborah E. Peruzzi, Niccolò Mead, Timothy J. Foulcer, Simon J. |
| AuthorAffiliation | a Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA d Department of Experimental Medical Science, and Wallenberg Center for Molecular Medicine Lund University and The Pediatric Heart Center, Skane University Hospital, Lund, Sweden f Sunnybrook Research Institute and Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada c University Hospitals Rainbow Babies and Children’s Hospital, Cleveland, OH, USA e SynOA Therapeutics, Philadelphia, PA 19119, USA b Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH, USA |
| AuthorAffiliation_xml | – name: c University Hospitals Rainbow Babies and Children’s Hospital, Cleveland, OH, USA – name: d Department of Experimental Medical Science, and Wallenberg Center for Molecular Medicine Lund University and The Pediatric Heart Center, Skane University Hospital, Lund, Sweden – name: e SynOA Therapeutics, Philadelphia, PA 19119, USA – name: f Sunnybrook Research Institute and Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada – name: a Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA – name: b Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH, USA |
| Author_xml | – sequence: 1 givenname: Timothy J. orcidid: 0000-0003-1891-3652 surname: Mead fullname: Mead, Timothy J. email: tjm192@case.edu organization: Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA – sequence: 2 givenname: Sumit orcidid: 0000-0002-5274-5122 surname: Bhutada fullname: Bhutada, Sumit organization: Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA – sequence: 3 givenname: Simon J. surname: Foulcer fullname: Foulcer, Simon J. organization: Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA – sequence: 4 givenname: Niccolò orcidid: 0000-0002-2929-4247 surname: Peruzzi fullname: Peruzzi, Niccolò organization: Department of Experimental Medical Science, and Wallenberg Center for Molecular Medicine Lund University and The Pediatric Heart Center, Skane University Hospital, Lund, Sweden – sequence: 5 givenname: Courtney M. surname: Nelson fullname: Nelson, Courtney M. organization: Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA – sequence: 6 givenname: Deborah E. orcidid: 0000-0001-9247-1122 surname: Seifert fullname: Seifert, Deborah E. organization: Department of Pediatrics, Case Western Reserve University School of Medicine, Cleveland, OH, USA – sequence: 7 givenname: Jonathan orcidid: 0000-0002-1202-9287 surname: Larkin fullname: Larkin, Jonathan organization: SynOA Therapeutics, Philadelphia, PA 19119, USA – sequence: 8 givenname: Karin surname: Tran-Lundmark fullname: Tran-Lundmark, Karin organization: Department of Experimental Medical Science, and Wallenberg Center for Molecular Medicine Lund University and The Pediatric Heart Center, Skane University Hospital, Lund, Sweden – sequence: 9 givenname: Jorge surname: Filmus fullname: Filmus, Jorge organization: Sunnybrook Research Institute and Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada – sequence: 10 givenname: Suneel S. orcidid: 0000-0001-8441-1226 surname: Apte fullname: Apte, Suneel S. email: aptes@ccf.org organization: Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38750698$$D View this record in MEDLINE/PubMed https://lup.lub.lu.se/record/8f932a41-d1f3-49af-9b0a-f6889032f8e8$$DView record from Swedish Publication Index oai:portal.research.lu.se:publications/8f932a41-d1f3-49af-9b0a-f6889032f8e8$$DView record from Swedish Publication Index |
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| Copyright | 2024 The Author(s) Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved. |
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| CorporateAuthor | Vessel Wall Biology WCMM- Wallenberg center för molekylär medicinsk forskning Department of Experimental Medical Science Kärlväggsbiologi Faculty of Medicine Lunds universitet Institutionen för experimentell medicinsk vetenskap Medicinska fakulteten WCMM-Wallenberg Centre for Molecular Medicine Lund University |
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| Keywords | Proteoglycan Metalloprotease Glypican Terminomics Degradomics Versican |
| Language | English |
| License | This is an open access article under the CC BY license. Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). |
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| Snippet | • Combined genetic-pharmacologic ADAMTS1 and ADAMTS5 inactivation in mice.• Degradomics identification of putative ADAMTS1 and ADAMTS5 substrates.• A... Extracellular matrix remodeling mechanisms are understudied in cardiac development and congenital heart defects. We show that matrix-degrading metalloproteases... |
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| SubjectTerms | ADAMTS1 Protein - genetics ADAMTS1 Protein - metabolism ADAMTS5 Protein - genetics ADAMTS5 Protein - metabolism Animals Degradomics Gene Expression Regulation, Developmental Glypican Glypicans - genetics Glypicans - metabolism Heart - growth & development Heart Defects, Congenital - genetics Heart Defects, Congenital - metabolism Heart Defects, Congenital - pathology Medical and Health Sciences Medical Biotechnology Medicin och hälsovetenskap Medicinsk bioteknologi Metalloprotease Mice Mice, Knockout Proteoglycan Proteolysis Terminomics Versican Versicans - genetics Versicans - metabolism |
| Title | Combined genetic-pharmacologic inactivation of tightly linked ADAMTS proteases in temporally specific windows uncovers distinct roles for versican proteolysis and glypican-6 in cardiac development |
| URI | https://dx.doi.org/10.1016/j.matbio.2024.05.003 https://www.ncbi.nlm.nih.gov/pubmed/38750698 https://www.proquest.com/docview/3055892357 https://pubmed.ncbi.nlm.nih.gov/PMC11526477 https://lup.lub.lu.se/record/8f932a41-d1f3-49af-9b0a-f6889032f8e8 oai:portal.research.lu.se:publications/8f932a41-d1f3-49af-9b0a-f6889032f8e8 |
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