DILTIAZEM AND VERAPAMIL PROTECT DYSTROPHIN-DEFICIENT MUSCLE FIBERS OF MDX MICE FROM DEGENERATION: A POTENTIAL ROLE IN CALCIUM BUFFERING AND SARCOLEMMAL STABILITY

dc.creatorMatsumura, CY
dc.creatorPertille, A
dc.creatorAlbuquerque, TCP
dc.creatorNeto, HS
dc.creatorMarques, MJ
dc.date2009
dc.dateFEB
dc.date2014-11-14T08:53:31Z
dc.date2015-11-26T17:14:09Z
dc.date2014-11-14T08:53:31Z
dc.date2015-11-26T17:14:09Z
dc.date.accessioned2018-03-29T00:02:29Z
dc.date.available2018-03-29T00:02:29Z
dc.identifierMuscle & Nerve. John Wiley & Sons Inc, v. 39, n. 2, n. 167, n. 176, 2009.
dc.identifier0148-639X
dc.identifierWOS:000262837700007
dc.identifier10.1002/mus.21188
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/61891
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/61891
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/61891
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1281742
dc.descriptionThe lack of dystrophin in mdx mice and in Duchenne muscular dystrophy causes sarcolemmal breakdown and increased calcium influx followed by myonecrosis. We examined whether the calcium channel blockers diltiazem and verapamil protect dystrophic muscles from degeneration. Mdx mice received daily intraperitoneal injections of diltiazem or verapamil for 18 days, followed by removal of the sternomastoid, diaphragm, fibialis anterior, and cardiac muscles. Control mdx mice were injected with saline. Both drugs significantly decreased blood creatine kinase levels. Total calcium content was significantly higher in mdx muscles than in control C57BI/10. Verapamil and diltiazem reduced total calcium content only in diaphragm and cardiac muscle. Histological analysis showed that diltiazem significantly attenuated myonecrosis in diaphragm. Immunoblots showed a significant increase of calsequestrin and P-dystroglycan levels in some diltiazem- and verapamil-treated muscles. Possible interactions of these drugs with the sarcoplasmic reticulum and sarcolemma may also contribute to the improvement of the dystrophic phenotype.
dc.description39
dc.description2
dc.description167
dc.description176
dc.languageen
dc.publisherJohn Wiley & Sons Inc
dc.publisherHoboken
dc.publisherEUA
dc.relationMuscle & Nerve
dc.relationMuscle Nerve
dc.rightsfechado
dc.rightshttp://olabout.wiley.com/WileyCDA/Section/id-406071.html
dc.sourceWeb of Science
dc.subjectBeta-dystroglycan
dc.subjectcalcium
dc.subjectcalsequestrin
dc.subjectdiltiazem
dc.subjectEvans blue dye
dc.subjectmdx
dc.subjectmuscle degeneration
dc.subjectverapamil
dc.subjectDuchenne Muscular-dystrophy
dc.subjectGrowth-factor-i
dc.subjectSkeletal-muscle
dc.subjectSarcoplasmic-reticulum
dc.subjectMouse Model
dc.subjectExpression
dc.subjectChannels
dc.subjectCalsequestrin
dc.subjectPhenotype
dc.subjectNecrosis
dc.titleDILTIAZEM AND VERAPAMIL PROTECT DYSTROPHIN-DEFICIENT MUSCLE FIBERS OF MDX MICE FROM DEGENERATION: A POTENTIAL ROLE IN CALCIUM BUFFERING AND SARCOLEMMAL STABILITY
dc.typeArtículos de revistas


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