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Large1 gene transfer in older myd mice with severe muscular dystrophy restores muscle function and greatly improves survival
Journal article   Open access   Peer reviewed

Large1 gene transfer in older myd mice with severe muscular dystrophy restores muscle function and greatly improves survival

Takahiro Yonekawa, Adam J. Rauckhorst, Sara El-Hattab, Marco A. Cuellar, David Venzke, Mary E. Anderson, Hidehiko Okuma, Alvin D. Pewa, Eric B. Taylor and Kevin P. Campbell
Science advances, Vol.8(21), pp.eabn0379-eabn0379
05/27/2022
DOI: 10.1126/sciadv.abn0379
PMCID: PMC9132445
PMID: 35613260
url
https://doi.org/10.1126/sciadv.abn0379View
Published (Version of record) Open Access

Abstract

Muscular dystrophy is a progressive and ultimately lethal neuromuscular disease. Although gene editing and gene transfer hold great promise as therapies when administered before the onset of severe clinical symptoms, it is unclear whether these strategies can restore muscle function and improve survival in the late stages of muscular dystrophy. Large myd /Large myd ( myd ) mice lack expression of like-acetylglucosaminyltransferase-1 ( Large1 ) and exhibit severe muscle pathophysiology, impaired mobility, and a markedly reduced life span. Here, we show that systemic delivery of AAV2/9 CMV Large1 (AAV Large1 ) in >34-week-old myd mice with advanced disease restores matriglycan expression on dystroglycan, attenuates skeletal muscle pathophysiology, improves motor and respiratory function, and normalizes systemic metabolism, which collectively and markedly extends survival. Our results in a mouse model of muscular dystrophy demonstrate that skeletal muscle function can be restored, illustrating its remarkable plasticity, and that survival can be greatly improved even after the onset of severe muscle pathophysiology. Large1 gene transfer improves muscle function and extends survival in older mice with severe muscular dystrophy.

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