Agrin Promotes Coordinated Therapeutic Processes Leading to Improved Cardiac Repair in Pigs.


Journal

Circulation
ISSN: 1524-4539
Titre abrégé: Circulation
Pays: United States
ID NLM: 0147763

Informations de publication

Date de publication:
09 2020
Historique:
pubmed: 9 6 2020
medline: 1 9 2021
entrez: 9 6 2020
Statut: ppublish

Résumé

Ischemic heart diseases are leading causes of death and reduced life quality worldwide. Although revascularization strategies significantly reduce mortality after acute myocardial infarction (MI), a large number of patients with MI develop chronic heart failure over time. We previously reported that a fragment of the extracellular matrix protein agrin promotes cardiac regeneration after MI in adult mice. To test the therapeutic potential of agrin in a preclinical porcine model, we performed ischemia-reperfusion injuries using balloon occlusion for 60 minutes followed by a 3-, 7-, or 28-day reperfusion period. We demonstrated that local (antegrade) delivery of recombinant human agrin to the infarcted pig heart can target the affected regions in an efficient and clinically relevant manner. A single dose of recombinant human agrin improved heart function, infarct size, fibrosis, and adverse remodeling parameters 28 days after MI. Short-term MI experiments along with complementary murine studies revealed myocardial protection, improved angiogenesis, inflammatory suppression, and cell cycle reentry as agrin's mechanisms of action. A single dose of agrin is capable of reducing ischemia-reperfusion injury and improving heart function, demonstrating that agrin could serve as a therapy for patients with acute MI and potentially heart failure.

Sections du résumé

BACKGROUND
Ischemic heart diseases are leading causes of death and reduced life quality worldwide. Although revascularization strategies significantly reduce mortality after acute myocardial infarction (MI), a large number of patients with MI develop chronic heart failure over time. We previously reported that a fragment of the extracellular matrix protein agrin promotes cardiac regeneration after MI in adult mice.
METHODS
To test the therapeutic potential of agrin in a preclinical porcine model, we performed ischemia-reperfusion injuries using balloon occlusion for 60 minutes followed by a 3-, 7-, or 28-day reperfusion period.
RESULTS
We demonstrated that local (antegrade) delivery of recombinant human agrin to the infarcted pig heart can target the affected regions in an efficient and clinically relevant manner. A single dose of recombinant human agrin improved heart function, infarct size, fibrosis, and adverse remodeling parameters 28 days after MI. Short-term MI experiments along with complementary murine studies revealed myocardial protection, improved angiogenesis, inflammatory suppression, and cell cycle reentry as agrin's mechanisms of action.
CONCLUSIONS
A single dose of agrin is capable of reducing ischemia-reperfusion injury and improving heart function, demonstrating that agrin could serve as a therapy for patients with acute MI and potentially heart failure.

Identifiants

pubmed: 32508131
doi: 10.1161/CIRCULATIONAHA.119.045116
doi:

Substances chimiques

Agrin 0
Recombinant Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

868-881

Auteurs

Andrea Baehr (A)

I Medizinische Klinik & Poliklinik, University Clinic Rechts der Isar, Technical University Munich, Germany (A.B., V.J., K.K., T.B., N.H., K.L.L., R.H., C.K.).
DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).

Kfir Baruch Umansky (KB)

The Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel (K.B.U., E.B., D.K., R.C.-R., E.T.).

Elad Bassat (E)

The Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel (K.B.U., E.B., D.K., R.C.-R., E.T.).

Victoria Jurisch (V)

I Medizinische Klinik & Poliklinik, University Clinic Rechts der Isar, Technical University Munich, Germany (A.B., V.J., K.K., T.B., N.H., K.L.L., R.H., C.K.).
DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).

Katharina Klett (K)

I Medizinische Klinik & Poliklinik, University Clinic Rechts der Isar, Technical University Munich, Germany (A.B., V.J., K.K., T.B., N.H., K.L.L., R.H., C.K.).
DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).

Tarik Bozoglu (T)

I Medizinische Klinik & Poliklinik, University Clinic Rechts der Isar, Technical University Munich, Germany (A.B., V.J., K.K., T.B., N.H., K.L.L., R.H., C.K.).
DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).

Nadja Hornaschewitz (N)

I Medizinische Klinik & Poliklinik, University Clinic Rechts der Isar, Technical University Munich, Germany (A.B., V.J., K.K., T.B., N.H., K.L.L., R.H., C.K.).
DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).

Olga Solyanik (O)

Department of Radiology, Klinikum Großhadern (O.S., C.C.), LMU Munich, Germany.

David Kain (D)

The Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel (K.B.U., E.B., D.K., R.C.-R., E.T.).

Bartolo Ferraro (B)

Institute for Cardiovascular Prevention (B.F., O.S.), LMU Munich, Germany.

Renee Cohen-Rabi (R)

The Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel (K.B.U., E.B., D.K., R.C.-R., E.T.).

Markus Krane (M)

Department of Surgery, German Heart Center Munich, Germany (M.K.).

Clemens Cyran (C)

Department of Radiology, Klinikum Großhadern (O.S., C.C.), LMU Munich, Germany.

Oliver Soehnlein (O)

DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).
Institute for Cardiovascular Prevention (B.F., O.S.), LMU Munich, Germany.

Karl Ludwig Laugwitz (KL)

I Medizinische Klinik & Poliklinik, University Clinic Rechts der Isar, Technical University Munich, Germany (A.B., V.J., K.K., T.B., N.H., K.L.L., R.H., C.K.).
DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).

Rabea Hinkel (R)

I Medizinische Klinik & Poliklinik, University Clinic Rechts der Isar, Technical University Munich, Germany (A.B., V.J., K.K., T.B., N.H., K.L.L., R.H., C.K.).
DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).
Department of Laboratory Animal Science, Deutsches Primatenzentrum GmbH, Leibniz-Institut für Primatenforschung, Göttingen, Germany (R.H.).

Christian Kupatt (C)

I Medizinische Klinik & Poliklinik, University Clinic Rechts der Isar, Technical University Munich, Germany (A.B., V.J., K.K., T.B., N.H., K.L.L., R.H., C.K.).
DZHK (German Center for Cardiovascular Research), partner site Munich Heart Alliance, Germany (A.B., V.J., K.K., T.B., N.H., B.F., O.S., K.L.L., R.H., C.K.).

Eldad Tzahor (E)

The Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel (K.B.U., E.B., D.K., R.C.-R., E.T.).

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