Growth hormone secretagogues modulate inflammation and fibrosis in mdx mouse model of Duchenne muscular dystrophy
Growth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentia...
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| Published in | Frontiers in immunology Vol. 14; p. 1119888 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Switzerland
Frontiers
2023
Frontiers Media S.A |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1664-3224 1664-3224 |
| DOI | 10.3389/fimmu.2023.1119888 |
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| Abstract | Growth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentially targeting multiple steps of pathogenic cascade in Duchenne muscular dystrophy (DMD).
Here, we aimed to provide preclinical evidence for potential benefits of GHSs in DMD,
a multidisciplinary
and
comparison in
mice, of two
synthesized compounds (EP80317 and JMV2894), with a wide but different profile. 4-week-old
mice were treated for 8 weeks with EP80317 or JMV2894 (320 µg/kg/d, s.c.).
, both GHSs increased mice forelimb force (recovery score, RS towards WT: 20% for EP80317 and 32% for JMV2894 at week 8). In parallel, GHSs also reduced diaphragm (DIA) and gastrocnemius (GC) ultrasound echodensity, a fibrosis-related parameter (RS: ranging between 26% and 75%).
, both drugs ameliorated DIA isometric force and calcium-related indices (
, RS: 40% for tetanic force). Histological analysis highlighted a relevant reduction of fibrosis in GC and DIA muscles of treated mice, paralleled by a decrease in gene expression of
and
. Also, decreased levels of pro-inflammatory genes (
), accompanied by an increment in
and
expression, were observed in response to treatments, suggesting an overall improvement of myofiber metabolism. No detectable transcript levels of
, nor an increase of circulating IGF-1 were found, suggesting the presence of a novel receptor-independent mechanism in skeletal muscle. Preliminary docking studies revealed a potential binding capability of JMV2894 on metalloproteases involved in extracellular matrix remodeling and cytokine production, such as ADAMTS-5 and MMP-9, overactivated in DMD.
Our results support the interest of GHSs as modulators of pathology progression in
mice, disclosing a direct anti-fibrotic action that may prove beneficial to contrast pathological remodeling. |
|---|---|
| AbstractList | Growth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentially targeting multiple steps of pathogenic cascade in Duchenne muscular dystrophy (DMD).IntroductionGrowth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentially targeting multiple steps of pathogenic cascade in Duchenne muscular dystrophy (DMD).Here, we aimed to provide preclinical evidence for potential benefits of GHSs in DMD, via a multidisciplinary in vivo and ex vivo comparison in mdx mice, of two ad hoc synthesized compounds (EP80317 and JMV2894), with a wide but different profile. 4-week-old mdx mice were treated for 8 weeks with EP80317 or JMV2894 (320 µg/kg/d, s.c.).MethodsHere, we aimed to provide preclinical evidence for potential benefits of GHSs in DMD, via a multidisciplinary in vivo and ex vivo comparison in mdx mice, of two ad hoc synthesized compounds (EP80317 and JMV2894), with a wide but different profile. 4-week-old mdx mice were treated for 8 weeks with EP80317 or JMV2894 (320 µg/kg/d, s.c.).In vivo, both GHSs increased mice forelimb force (recovery score, RS towards WT: 20% for EP80317 and 32% for JMV2894 at week 8). In parallel, GHSs also reduced diaphragm (DIA) and gastrocnemius (GC) ultrasound echodensity, a fibrosis-related parameter (RS: ranging between 26% and 75%). Ex vivo, both drugs ameliorated DIA isometric force and calcium-related indices (e.g., RS: 40% for tetanic force). Histological analysis highlighted a relevant reduction of fibrosis in GC and DIA muscles of treated mice, paralleled by a decrease in gene expression of TGF-β1 and Col1a1. Also, decreased levels of pro-inflammatory genes (IL-6, CD68), accompanied by an increment in Sirt-1, PGC-1α and MEF2c expression, were observed in response to treatments, suggesting an overall improvement of myofiber metabolism. No detectable transcript levels of GHS receptor-1a, nor an increase of circulating IGF-1 were found, suggesting the presence of a novel receptor-independent mechanism in skeletal muscle. Preliminary docking studies revealed a potential binding capability of JMV2894 on metalloproteases involved in extracellular matrix remodeling and cytokine production, such as ADAMTS-5 and MMP-9, overactivated in DMD.ResultsIn vivo, both GHSs increased mice forelimb force (recovery score, RS towards WT: 20% for EP80317 and 32% for JMV2894 at week 8). In parallel, GHSs also reduced diaphragm (DIA) and gastrocnemius (GC) ultrasound echodensity, a fibrosis-related parameter (RS: ranging between 26% and 75%). Ex vivo, both drugs ameliorated DIA isometric force and calcium-related indices (e.g., RS: 40% for tetanic force). Histological analysis highlighted a relevant reduction of fibrosis in GC and DIA muscles of treated mice, paralleled by a decrease in gene expression of TGF-β1 and Col1a1. Also, decreased levels of pro-inflammatory genes (IL-6, CD68), accompanied by an increment in Sirt-1, PGC-1α and MEF2c expression, were observed in response to treatments, suggesting an overall improvement of myofiber metabolism. No detectable transcript levels of GHS receptor-1a, nor an increase of circulating IGF-1 were found, suggesting the presence of a novel receptor-independent mechanism in skeletal muscle. Preliminary docking studies revealed a potential binding capability of JMV2894 on metalloproteases involved in extracellular matrix remodeling and cytokine production, such as ADAMTS-5 and MMP-9, overactivated in DMD.Our results support the interest of GHSs as modulators of pathology progression in mdx mice, disclosing a direct anti-fibrotic action that may prove beneficial to contrast pathological remodeling.DiscussionOur results support the interest of GHSs as modulators of pathology progression in mdx mice, disclosing a direct anti-fibrotic action that may prove beneficial to contrast pathological remodeling. IntroductionGrowth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentially targeting multiple steps of pathogenic cascade in Duchenne muscular dystrophy (DMD).MethodsHere, we aimed to provide preclinical evidence for potential benefits of GHSs in DMD, via a multidisciplinary in vivo and ex vivo comparison in mdx mice, of two ad hoc synthesized compounds (EP80317 and JMV2894), with a wide but different profile. 4-week-old mdx mice were treated for 8 weeks with EP80317 or JMV2894 (320 µg/kg/d, s.c.).ResultsIn vivo, both GHSs increased mice forelimb force (recovery score, RS towards WT: 20% for EP80317 and 32% for JMV2894 at week 8). In parallel, GHSs also reduced diaphragm (DIA) and gastrocnemius (GC) ultrasound echodensity, a fibrosis-related parameter (RS: ranging between 26% and 75%). Ex vivo, both drugs ameliorated DIA isometric force and calcium-related indices (e.g., RS: 40% for tetanic force). Histological analysis highlighted a relevant reduction of fibrosis in GC and DIA muscles of treated mice, paralleled by a decrease in gene expression of TGF-β1 and Col1a1. Also, decreased levels of pro-inflammatory genes (IL-6, CD68), accompanied by an increment in Sirt-1, PGC-1α and MEF2c expression, were observed in response to treatments, suggesting an overall improvement of myofiber metabolism. No detectable transcript levels of GHS receptor-1a, nor an increase of circulating IGF-1 were found, suggesting the presence of a novel receptor-independent mechanism in skeletal muscle. Preliminary docking studies revealed a potential binding capability of JMV2894 on metalloproteases involved in extracellular matrix remodeling and cytokine production, such as ADAMTS-5 and MMP-9, overactivated in DMD.DiscussionOur results support the interest of GHSs as modulators of pathology progression in mdx mice, disclosing a direct anti-fibrotic action that may prove beneficial to contrast pathological remodeling. Growth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentially targeting multiple steps of pathogenic cascade in Duchenne muscular dystrophy (DMD). Here, we aimed to provide preclinical evidence for potential benefits of GHSs in DMD, a multidisciplinary and comparison in mice, of two synthesized compounds (EP80317 and JMV2894), with a wide but different profile. 4-week-old mice were treated for 8 weeks with EP80317 or JMV2894 (320 µg/kg/d, s.c.). , both GHSs increased mice forelimb force (recovery score, RS towards WT: 20% for EP80317 and 32% for JMV2894 at week 8). In parallel, GHSs also reduced diaphragm (DIA) and gastrocnemius (GC) ultrasound echodensity, a fibrosis-related parameter (RS: ranging between 26% and 75%). , both drugs ameliorated DIA isometric force and calcium-related indices ( , RS: 40% for tetanic force). Histological analysis highlighted a relevant reduction of fibrosis in GC and DIA muscles of treated mice, paralleled by a decrease in gene expression of and . Also, decreased levels of pro-inflammatory genes ( ), accompanied by an increment in and expression, were observed in response to treatments, suggesting an overall improvement of myofiber metabolism. No detectable transcript levels of , nor an increase of circulating IGF-1 were found, suggesting the presence of a novel receptor-independent mechanism in skeletal muscle. Preliminary docking studies revealed a potential binding capability of JMV2894 on metalloproteases involved in extracellular matrix remodeling and cytokine production, such as ADAMTS-5 and MMP-9, overactivated in DMD. Our results support the interest of GHSs as modulators of pathology progression in mice, disclosing a direct anti-fibrotic action that may prove beneficial to contrast pathological remodeling. Growth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance GH/insulin-like growth factor-1 (IGF-1)-mediated myogenesis, and to inhibit angiotensin-converting enzyme. These mechanisms are of interest for potentially targeting multiple steps of pathogenic cascade in Duchenne muscular dystrophy (DMD). Methods: Here, we aimed to provide preclinical evidence for potential benefits of GHSs in DMD, via a multidisciplinary in vivo and ex vivo comparison in mdx mice, of two ad hoc synthesized compounds (EP80317 and JMV2894), with a wide but different profile. 4-week-old mdx mice were treated for 8 weeks with EP80317 or JMV2894 (320 µg/kg/d, s.c.). Results: In vivo , both GHSs increased mice forelimb force (recovery score, RS towards WT: 20% for EP80317 and 32% for JMV2894 at week 8). In parallel, GHSs also reduced diaphragm (DIA) and gastrocnemius (GC) ultrasound echodensity, a fibrosis-related parameter (RS: ranging between 26% and 75%). Ex vivo , both drugs ameliorated DIA isometric force and calcium-related indices ( e.g. , RS: 40% for tetanic force). Histological analysis highlighted a relevant reduction of fibrosis in GC and DIA muscles of treated mice, paralleled by a decrease in gene expression of TGF-β1 and Col1a1 . Also, decreased levels of pro-inflammatory genes ( IL-6, CD68 ), accompanied by an increment in Sirt-1, PGC-1α and MEF2c expression, were observed in response to treatments, suggesting an overall improvement of myofiber metabolism. No detectable transcript levels of GHS receptor-1a , nor an increase of circulating IGF-1 were found, suggesting the presence of a novel receptor-independent mechanism in skeletal muscle. Preliminary docking studies revealed a potential binding capability of JMV2894 on metalloproteases involved in extracellular matrix remodeling and cytokine production, such as ADAMTS-5 and MMP-9, overactivated in DMD. Discussion: Our results support the interest of GHSs as modulators of pathology progression in mdx mice, disclosing a direct anti-fibrotic action that may prove beneficial to contrast pathological remodeling. |
| Author | Denoyelle, Severine Torsello, Antonio Mantuano, Paola Mele, Antonietta Cruciani, Gabriele De Luca, Annamaria Cappellari, Ornella Liantonio, Antonella Nicolotti, Orazio Boccanegra, Brigida Trisciuzzi, Daniela Fehrentz, Jean-Alain Sanarica, Francesca Cerchiara, Alessandro Giovanni Conte, Elena Meanti, Ramona Bresciani, Elena De Bellis, Michela Cirmi, Santa Tulimiero, Lisamaura Rizzi, Laura |
| AuthorAffiliation | 3 Institut des Biomolécules Max Mousseron, UMR 5247 CNRS-Université Montpellier-ENSCM, Faculté de Pharmacie , Montpellier , France 2 School of Medicine and Surgery, University of Milan-BICOCCA , Milan , Italy 4 Department of Chemistry, Biology and Biotechnology, University of Perugia , Perugia , Italy 1 Department of Pharmacy – Drug Sciences, University of Bari “Aldo Moro” , Bari , Italy |
| AuthorAffiliation_xml | – name: 3 Institut des Biomolécules Max Mousseron, UMR 5247 CNRS-Université Montpellier-ENSCM, Faculté de Pharmacie , Montpellier , France – name: 4 Department of Chemistry, Biology and Biotechnology, University of Perugia , Perugia , Italy – name: 2 School of Medicine and Surgery, University of Milan-BICOCCA , Milan , Italy – name: 1 Department of Pharmacy – Drug Sciences, University of Bari “Aldo Moro” , Bari , Italy |
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| Copyright | Copyright © 2023 Boccanegra, Cappellari, Mantuano, Trisciuzzi, Mele, Tulimiero, De Bellis, Cirmi, Sanarica, Cerchiara, Conte, Meanti, Rizzi, Bresciani, Denoyelle, Fehrentz, Cruciani, Nicolotti, Liantonio, Torsello and De Luca. Attribution Copyright © 2023 Boccanegra, Cappellari, Mantuano, Trisciuzzi, Mele, Tulimiero, De Bellis, Cirmi, Sanarica, Cerchiara, Conte, Meanti, Rizzi, Bresciani, Denoyelle, Fehrentz, Cruciani, Nicolotti, Liantonio, Torsello and De Luca 2023 Boccanegra, Cappellari, Mantuano, Trisciuzzi, Mele, Tulimiero, De Bellis, Cirmi, Sanarica, Cerchiara, Conte, Meanti, Rizzi, Bresciani, Denoyelle, Fehrentz, Cruciani, Nicolotti, Liantonio, Torsello and De Luca |
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| Keywords | fibrosis growth hormone secretagogues skeletal muscle mdx mouse Duchenne muscular dystrophy |
| Language | English |
| License | Copyright © 2023 Boccanegra, Cappellari, Mantuano, Trisciuzzi, Mele, Tulimiero, De Bellis, Cirmi, Sanarica, Cerchiara, Conte, Meanti, Rizzi, Bresciani, Denoyelle, Fehrentz, Cruciani, Nicolotti, Liantonio, Torsello and De Luca. Attribution: http://creativecommons.org/licenses/by This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Edited by: Kanneboyina Nagaraju, Binghamton University, United States This article was submitted to Inflammation, a section of the journal Frontiers in Immunology These authors have contributed equally to this work and share first authorship Reviewed by: Melissa Morales, Binghamton University, United States; Lucas Robert Smith, University of California, Davis, United States |
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| References | Gortan Cappellari (B22) 2017; 31 Reano (B24) 2017; 35 Zambelli (B52) 2021; 15 Friesner (B45) 2004; 47 Sun (B17) 2009; 280 Livak (B40) 2001; 25 Gamberi (B13) 2018; 18 van Putten (B39) 2019; 33 Kumar (B58) 2010; 177 Angelino (B21) 2015; 2015 Willmann (B5) 2015; 2 Capogrosso (B12) 2017; 122 De Luca (B10) 2003; 304 Torsello (B30) 2012; 66 De Luca (B6) 2005; 166 Angelino (B23) 2018; 62 Mele (B36) 2019; 204 Sirago (B29) 2017; 7 Mele (B38) 2021; 16 Siragusa (B47) 2015; 83 D’Angelo (B8) 2012; 65 Brebion (B41) 2021; 64 Spurney (B14) 2008; 18 Trisciuzzi (B50) 2022; 62 Mantuano (B35) 2021; 171 McDonald (B59) 2020; 127 Liu (B60) 2018; 98 Mantuano (B34) 2021; 11 Mantuano (B56) 2018; 154 Wren (B20) 2001; 86 Mantuano (B37) 2020; 12 Addinsall (B57) 2020; 10 Zhang (B54) 2016; 2016 Camerino (B11) 2014; 23 Sun (B49) 2007; 86 Cozzoli (B18) 2014; 307 Marleau (B55) 2005; 19 Xu (B51) 2012; 303 Liantonio (B28) 2013; 154 Durbeej (B2) 2002; 12 Rowsell (B42) 2002; 319 (B44) 2021 Khairallah (B9) 2012; 5 Moulin (B31) 2013; 44 Sanarica (B33) 2019; 145 Bianchi (B19) 2011; 21 De Vriese (B25) 2004; 145 Bushby (B4) 2010; 9 Conte (B26) 2020; 21 (B43) 2021 De Luca (B7) 2012; 31 Prosser (B15) 2013; 58 Pierno (B27) 2003; 139 Cohn (B16) 2007; 13 Hoffman (B3) 2001; 22 Muses (B48) 2011; 6 Duan (B1) 2021; 7 Capogrosso (B32) 2018; 32 Duddy (B53) 2015; 5 Siragusa (B46) 2014; 33 |
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| Snippet | Growth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance... IntroductionGrowth hormone secretagogues (GHSs) exert multiple actions, being able to activate GHS-receptor 1a, control inflammation and metabolism, to enhance... |
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| SubjectTerms | Animals Chemical Sciences Disease Models, Animal Duchenne muscular dystrophy Fibrosis Growth Hormone - pharmacology Growth Hormone - therapeutic use growth hormone secretagogues Human health and pathology Immunology Inflammation - drug therapy Inflammation - metabolism Inflammation - pathology Insulin-Like Growth Factor I - pharmacology Insulin-Like Growth Factor I - therapeutic use Life Sciences Male mdx mouse Medicinal Chemistry Mice Mice, Inbred mdx Muscular Dystrophy, Duchenne - metabolism Muscular Dystrophy, Duchenne - pathology Pharmaceutical sciences Pharmacology Secretagogues - metabolism skeletal muscle |
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| Title | Growth hormone secretagogues modulate inflammation and fibrosis in mdx mouse model of Duchenne muscular dystrophy |
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