Diltiazem improves contractile properties of skeletal muscle in dysferlin-deficient BLAJ mice, but does not reduce contraction-induced muscle damage
Date
2018Journal
Physiological ReportsPublisher
American Physiological SocietyType
Article
Metadata
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B6.A‐Dysfprmd/GeneJ (BLAJ) mice model human limb‐girdle muscular dystrophy 2B (LGMD2B), which is linked to mutations in the dysferlin (DYSF) gene. We tested the hypothesis that, the calcium ion (Ca2+) channel blocker diltiazem (DTZ), reduces contraction‐induced skeletal muscle damage, in BLAJ mice. We randomly assigned mice (N = 12; 3–4 month old males) to one of two groups – DTZ (N = 6) or vehicle (VEH, distilled water, N = 6). We conditioned mice with either DTZ or VEH for 1 week, after which, their tibialis anterior (TA) muscles were tested for contractile torque and susceptibility to injury from forced eccentric contractions. We continued dosing with DTZ or VEH for 3 days following eccentric contractions, and then studied torque recovery and muscle damage. We analyzed contractile torque before eccentric contractions, immediately after eccentric contractions, and at 3 days after eccentric contractions; and counted damaged fibers in the injured and uninjured TA muscles. We found that DTZ improved contractile torque before and immediately after forced eccentric contractions, but did not reduce delayed‐onset muscle damage that was observed at 3 days after eccentric contractions. Copyright 2018 The Authors.Sponsors
This work was directly supported by the following awards to JAR: research grants from the Jain Foundation Inc., a Faculty Research Awards Program (FRAP) grant from the Eugene Applebaum College of Pharmacy and Health Sciences at Wayne State University, and a faculty startup package from Wayne State University.Identifier to cite or link to this item
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85048468391&doi=10.14814%2fphy2.13727&partnerID=40&md5=cd21de6260c94d49699f04e966b1bb79; http://hdl.handle.net/10713/9156ae974a485f413a2113503eed53cd6c53
10.14814/phy2.13727