Intracellular pH regulation in isolated fast-twitch skeletal muscle from dystrophin-deficient mouse.

Decostre, V;Gailly, Philippe;Debaix, Huguette;Colson-Van Schoor, M;Gillis, Jean-Marie;et.al.
(2002) Neuromuscular Disorders — Vol. 12, n° 5, p. 447-456 (2002)

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Authors
  • Decostre, VUCLouvain
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  • Author
  • Debaix, HuguetteUCLouvain
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  • Colson-Van Schoor, MUCLouvain
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  • Cao, M LUCLouvain
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  • Gillis, Jean-MarieUCLouvain
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Abstract
In muscles from anaesthetized dystrophin-deficient mdx mice, exercise results in a stronger acidification and a slower intracellular pH recovery compared to control mice. We examined whether this observation could be attributed to defective H+-carriers in dystrophin-lacking muscles. Immunohistochemistry and Western blots revealed no defect in mdx muscles for the presence of the lactate-/H+co-transporter MCT4 and of the Na+/H+ antiporter NHE1, the main H+-carriers active in fast-twitch skeletal muscle after exercise. Functional tests of the H+-transporters, on isolated muscles submitted to identical flow of superfusion, were performed in conditions meant to lower intracellular pH: repetitive electrical stimulation or NH4Cl pre-pulse. These revealed no defect in intracellular pH recovery in mdx muscles. Therefore, we conclude that impaired intracellular pH regulation in anaesthetized mdx mice is not attributable to a reduced presence or activity of H+-extruders. We propose that CO2 washout might be slowed down in vivo in mdx muscles because of the defective vascular response in contracting muscles from these mice.
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Decostre, V., Gailly, P., Debaix, H., Colson-Van Schoor, M., Cao, M. L., & Gillis, J.-M. (2002). Intracellular pH regulation in isolated fast-twitch skeletal muscle from dystrophin-deficient mouse. Neuromuscular Disorders, 12(5), 447-456. https://doi.org/10.1016/S0960-8966(01)00304-2 (Original work published 2002)