Enhanced expression of the human Survival motor neuron 1 gene from a codon-optimised cDNA transgene in vitro and in vivo.


Journal

Gene therapy
ISSN: 1476-5462
Titre abrégé: Gene Ther
Pays: England
ID NLM: 9421525

Informations de publication

Date de publication:
15 Jun 2023
Historique:
received: 20 04 2022
accepted: 04 05 2023
revised: 14 04 2023
medline: 16 6 2023
pubmed: 16 6 2023
entrez: 15 6 2023
Statut: aheadofprint

Résumé

Spinal muscular atrophy (SMA) is a neuromuscular disease particularly characterised by degeneration of ventral motor neurons. Survival motor neuron (SMN) 1 gene mutations cause SMA, and gene addition strategies to replace the faulty SMN1 copy are a therapeutic option. We have developed a novel, codon-optimised hSMN1 transgene and produced integration-proficient and integration-deficient lentiviral vectors with cytomegalovirus (CMV), human synapsin (hSYN) or human phosphoglycerate kinase (hPGK) promoters to determine the optimal expression cassette configuration. Integrating, CMV-driven and codon-optimised hSMN1 lentiviral vectors resulted in the highest production of functional SMN protein in vitro. Integration-deficient lentiviral vectors also led to significant expression of the optimised transgene and are expected to be safer than integrating vectors. Lentiviral delivery in culture led to activation of the DNA damage response, in particular elevating levels of phosphorylated ataxia telangiectasia mutated (pATM) and γH2AX, but the optimised hSMN1 transgene showed some protective effects. Neonatal delivery of adeno-associated viral vector (AAV9) vector encoding the optimised transgene to the Smn

Identifiants

pubmed: 37322133
doi: 10.1038/s41434-023-00406-0
pii: 10.1038/s41434-023-00406-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Spinal Muscular Atrophy Trust (SMA Trust)
ID : UK SMA Research Consortium
Organisme : SMA Trust (Spinal Muscular Atrophy Trust)
ID : UK SMA Research Consortium
Organisme : SMA Trust (Spinal Muscular Atrophy Trust)
ID : UK SMA Research Consortium
Organisme : Great Ormond Street Hospital Charity (GOSH)
ID : V5018
Organisme : Great Ormond Street Hospital Charity (GOSH)
ID : V5018

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Neda A M Nafchi (NAM)

AGCTlab.org, Centre of Gene and Cell Therapy, Centre for Biomedical Sciences, Department of Biological Sciences, School of Life Sciences and the Environment, Royal Holloway University of London, Egham, TW20 0EX, UK.

Ellie M Chilcott (EM)

AGCTlab.org, Centre of Gene and Cell Therapy, Centre for Biomedical Sciences, Department of Biological Sciences, School of Life Sciences and the Environment, Royal Holloway University of London, Egham, TW20 0EX, UK.

Sharon Brown (S)

School of Pharmacy and Bioengineering, Keele University, Staffordshire, ST5 5BG, UK.
Wolfson Centre for Inherited Neuromuscular Disease, TORCH Building, RJAH Orthopaedic Hospital, Oswestry, SY10 7AG, UK.

Heidi R Fuller (HR)

School of Pharmacy and Bioengineering, Keele University, Staffordshire, ST5 5BG, UK.
Wolfson Centre for Inherited Neuromuscular Disease, TORCH Building, RJAH Orthopaedic Hospital, Oswestry, SY10 7AG, UK.

Melissa Bowerman (M)

Wolfson Centre for Inherited Neuromuscular Disease, TORCH Building, RJAH Orthopaedic Hospital, Oswestry, SY10 7AG, UK.
School of Medicine, Keele University, Staffordshire, ST5 5BG, UK.

Rafael J Yáñez-Muñoz (RJ)

AGCTlab.org, Centre of Gene and Cell Therapy, Centre for Biomedical Sciences, Department of Biological Sciences, School of Life Sciences and the Environment, Royal Holloway University of London, Egham, TW20 0EX, UK. rafael.yanez@royalholloway.ac.uk.

Classifications MeSH