Inhibition of Activin Receptor Type IIB Increases Strength and Lifespan in Myotubularin-Deficient Mice

X-linked myotubular myopathy (XLMTM) is a congenital disorder caused by deficiency of the lipid phosphatase, myotubularin. Patients with XLMTM often have severe perinatal weakness that requires mechanical ventilation to prevent death from respiratory failure. Muscle biopsy specimens from patients wi...

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Veröffentlicht in:Am J Pathol 2011-02, Vol.178 (2), p.784-793
Hauptverfasser: Lawlor, Michael W, Read, Benjamin P, Edelstein, Rachel, Yang, Nicole, Pierson, Christopher R, Stein, Matthew J, Wermer-Colan, Ariana, Buj-Bello, Anna, Lachey, Jennifer L, Seehra, Jasbir S, Beggs, Alan H
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container_start_page 784
container_title Am J Pathol
container_volume 178
creator Lawlor, Michael W
Read, Benjamin P
Edelstein, Rachel
Yang, Nicole
Pierson, Christopher R
Stein, Matthew J
Wermer-Colan, Ariana
Buj-Bello, Anna
Lachey, Jennifer L
Seehra, Jasbir S
Beggs, Alan H
description X-linked myotubular myopathy (XLMTM) is a congenital disorder caused by deficiency of the lipid phosphatase, myotubularin. Patients with XLMTM often have severe perinatal weakness that requires mechanical ventilation to prevent death from respiratory failure. Muscle biopsy specimens from patients with XLMTM exhibit small myofibers with central nuclei and central aggregations of organelles in many cells. It was postulated that therapeutically increasing muscle fiber size would cause symptomatic improvement in myotubularin deficiency. Recent studies have elucidated an important role for the activin-receptor type IIB (ActRIIB) in regulation of muscle growth and have demonstrated that ActRIIB inhibition results in significant muscle hypertrophy. To evaluate whether promoting muscle hypertrophy can attenuate symptoms resulting from myotubularin deficiency, the effect of ActRIIB-mFC treatment was determined in myotubularin-deficient ( Mtm1 δ4) mice. Compared with wild-type mice, untreated Mtm1 δ4 mice have decreased body weight, skeletal muscle hypotrophy, and reduced survival. Treatment of Mtm1 δ4 mice with ActRIIB-mFC produced a 17% extension of lifespan, with transient increases in weight, forelimb grip strength, and myofiber size. Pathologic analysis of Mtm1δ4 mice during treatment revealed that ActRIIB-mFC produced marked hypertrophy restricted to type 2b myofibers, which suggests that oxidative fibers in Mtm1δ4 animals are incapable of a hypertrophic response in this setting. These results support ActRIIB-mFC as an effective treatment for the weakness observed in myotubularin deficiency.
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Treatment of Mtm1 δ4 mice with ActRIIB-mFC produced a 17% extension of lifespan, with transient increases in weight, forelimb grip strength, and myofiber size. Pathologic analysis of Mtm1δ4 mice during treatment revealed that ActRIIB-mFC produced marked hypertrophy restricted to type 2b myofibers, which suggests that oxidative fibers in Mtm1δ4 animals are incapable of a hypertrophic response in this setting. 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subjects Activin Receptors, Type II - antagonists & inhibitors
Activin Receptors, Type II - metabolism
Animals
Behavior, Animal - drug effects
Biological and medical sciences
Body Weight - drug effects
Forelimb - drug effects
Forelimb - physiology
Gravitation
Hand Strength - physiology
Investigative techniques, diagnostic techniques (general aspects)
Life Sciences
Longevity - drug effects
Longevity - physiology
Medical sciences
Mice
Mice, Inbred C57BL
Muscle Strength - drug effects
Muscle Strength - physiology
Muscle, Skeletal - drug effects
Muscle, Skeletal - metabolism
Muscle, Skeletal - pathology
Muscle, Skeletal - ultrastructure
Myostatin - metabolism
Pathology
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Protein Tyrosine Phosphatases, Non-Receptor - deficiency
Protein Tyrosine Phosphatases, Non-Receptor - metabolism
Recombinant Fusion Proteins - pharmacology
Regular
Survival Analysis
title Inhibition of Activin Receptor Type IIB Increases Strength and Lifespan in Myotubularin-Deficient Mice
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