Li Yue1, M A Hassan Talukder2, Anagha Gurjar2, Jung Il Lee3, Mark Noble4, Robert T Dirksen5, Joe Chakkalakal6, John C Elfar2. 1. Department of Orthopaedics, The Warren Alpert Medical School of Brown University/Rhode Island Hospital, Providence, Rhode Island, USA. 2. Department of Orthopaedics and Rehabilitation, Center for Orthopaedics and Translational Science, The Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, 500 University Drive, Mail Code H089, Hershey, Pennsylvania, 17033, USA. 3. Department of Orthopaedic Surgery, Hanyang University Guri Hospital, South Korea. 4. Department of Biomedical Genetics, The University of Rochester Medical Center Rochester, New York, USA. 5. Department of Pharmacology & Physiology, The University of Rochester Medical Center Rochester, New York, USA. 6. Department of Pharmacology and Physiology and Biomedical Engineering, The University of Rochester Medical Center Rochester, New York, USA.
Abstract
INTRODUCTION: We recently demonstrated the beneficial effects of 4-aminopyridine (4-AP), a potassium channel blocker, in enhancing remyelination and recovery of nerve conduction velocity and motor function after sciatic nerve crush injury in mice. Although muscle atrophy occurs very rapidly after nerve injury, the effect of 4-AP on muscle atrophy and intrinsic muscle contractile function is largely unknown. METHODS: Mice were assigned to sciatic nerve crush injury and no-injury groups and were followed for 3, 7, and 14 days with/without 4-AP or saline treatment. Morphological, functional, and transcriptional properties of skeletal muscle were assessed. RESULTS: In addition to improving in vivo function, 4-AP significantly reduced muscle atrophy with increased muscle fiber diameter and contractile force. Reduced muscle atrophy was associated with attenuated expression of atrophy-related genes and increased expression of proliferating stem cells. DISCUSSION: These findings provide new insights into the potential therapeutic benefits of 4-AP against nerve injury-induced muscle atrophy and dysfunction. Muscle Nerve 60: 192-201, 2019.
INTRODUCTION: We recently demonstrated the beneficial effects of 4-aminopyridine (4-AP), a potassium channel blocker, in enhancing remyelination and recovery of nerve conduction velocity and motor function after sciatic nerve crush injury in mice. Although muscle atrophy occurs very rapidly after nerve injury, the effect of 4-AP on muscle atrophy and intrinsic muscle contractile function is largely unknown. METHODS:Mice were assigned to sciatic nerve crush injury and no-injury groups and were followed for 3, 7, and 14 days with/without 4-AP or saline treatment. Morphological, functional, and transcriptional properties of skeletal muscle were assessed. RESULTS: In addition to improving in vivo function, 4-AP significantly reduced muscle atrophy with increased muscle fiber diameter and contractile force. Reduced muscle atrophy was associated with attenuated expression of atrophy-related genes and increased expression of proliferating stem cells. DISCUSSION: These findings provide new insights into the potential therapeutic benefits of 4-AP against nerve injury-induced muscle atrophy and dysfunction. Muscle Nerve 60: 192-201, 2019.
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