Letters to the editor

Lefaucheur, Jean Pascal; Sebille, Alain; Boland, Benoît; Himpens, Bernard; Denef, J. C.; Gillis, Jean-Marie; Ikeda, Ken; Kinoshita, Masao; Iwasaki, Yasuo; Tremblay, Jacques P.; Poersch, Marius; K�ster, B.; McManis, Philip G.; Gominak, Stasha; Siegel, Irwin M.; Fitzmaurice, Paul S.; Shaw, Ian C.; Kleiner, H; Miller, R; Monks, T J; Lau, S S; Mitchell, John D.; Lynch, Patrick; Ando, Yukio; Yonemitsu, Mizue; Uchino, Makoto; Ando, Masayuki; Felice, Kevin J.; Relva, Gretchen M.

doi:10.1002/mus.880190602

Muscle Nerve

1996

DOI: 10.1002/mus.880190602

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Letters to the editor

Jean Pascal Lefaucheur

Alain Sebille

Benoît Boland³

et al.

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Dmdmdx-βgeo: A new allele for the mouse dystrophin gene

Wertz

Füchtbauer

1998

Dev. Dyn.

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During a gene trap screen, an insertion of the gene trap vector into the dystrophin gene, creating a new allele for the Dmd gene, has been discovered. Because the ROSAβgeo vector was used, the new allele is called Dmdmdx‐βgeo. The insertion occurred 3′ of exon 63 of the dystrophin gene, resulting in a mutation that affects all presently known dystrophin isoforms. In contrast to spontaneous or ENU‐induced alleles, Dmdmdx‐βgeo can be used to follow dystrophin expression by staining for β‐galactosidase activity. The high sensitivity of this method revealed additional and earlier expression of dystrophin during embryogenesis than that seen previously with other methods. Dystrophin promoters are active predominantly in the dermamyotome, limb buds, telencephalon, floor plate, eye, liver, pancreas anlagen, and cardiovascular system. Adult Dmdmdx‐βgeo mice show reporter gene expression in brain, eye, liver, pancreas, and lung. In skeletal and heart muscle, β‐galactosidase activity is not detectable, confirming Western blot data that indicate the absence of the mutant full‐length protein in these tissues. Hemizygous Dmdmdx‐βgeo mice show muscular dystrophy with degenerating muscle fibers, cellular infiltration, and regenerated muscle fibers that have centrally located nuclei. Some mutant animals develop a dilated esophagus, probably due to constriction by the hypertrophic crura of the diaphragm. Dev. Dyn. 1998;212:229–241. © 1998 Wiley‐Liss, Inc.

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Dmdmdx-βgeo: A new allele for the mouse dystrophin gene

Wertz

Füchtbauer

1998

Dev. Dyn.

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Gender dimorphism influences extracellular matrix expression and regeneration of muscular tissue in mdx dystrophic mice

Salimena

Lagrota-Candido

Quirico-Santos

2000

Histochem Cell Biol

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Mdx mouse, the animal model of Duchenne muscular dystrophy, lacks dystrophin and develops an X-linked recessive inflammatory myopathy characterized by degeneration of skeletal muscle fibers and connective tissue replacement. The present work aimed to assess whether gender dimorphism in mdx mice would influence skeletal muscle pathology at ages corresponding to main histological changes in the microenvironment of muscular tissue: myonecrosis, regeneration, and fibrosis. At the height of myonecrosis (6 weeks postnatal), skeletal muscles of male mdx mice showed increased sarcolemmal permeability, numerous inflammatory foci, and marked deposition of the extracellular matrix components (ECM) type I collagen and laminin. In contrast, age-matched mdx females showed mild ECM deposition, discrete myonecrosis, but increased numbers of regenerating fibers expressing the satellite cell marker NCAM. In contrast ovariectomized mdx females showed decreased numbers of regenerating fibers. Older (24 and 48 weeks postnatal) mdx females showed extensive fibrosis with increased sarcolemmal permeability and marked deposition of ECM components than corresponding males. These results suggest a role for female hormones in the control of myonecrosis probably by promoting regeneration of muscular tissue and mitigating inflammation especially at ages under the critical influence of sex hormones.

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Letters to the editor

Cited by 2 publications

References 40 publications

Dmdmdx-βgeo: A new allele for the mouse dystrophin gene

Dmdmdx-βgeo: A new allele for the mouse dystrophin gene

Gender dimorphism influences extracellular matrix expression and regeneration of muscular tissue in mdx dystrophic mice

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