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Maintenance of myonuclear domain during mechanical ventilation induced diaphragmatic atrophy
Author(s) -
McClung Joseph Matthew,
Kavazis Andreas N,
DeRuisseau Keith,
Falk Darin,
Deering Melissa,
Lee Youngil,
Powers Scott
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb32
Subject(s) - tunel assay , diaphragm (acoustics) , diaphragmatic breathing , atrophy , apoptosis , chemistry , medicine , endocrinology , pathology , physics , biochemistry , alternative medicine , acoustics , loudspeaker
Unloading the diaphragm via mechanical ventilation (MV) results in rapid diaphragmatic fiber atrophy. We tested the hypothesis that MV‐induced diaphragmatic atrophy is associated with a loss of myonuclei via an apoptotic‐like mechanism resulting in a constant myonuclear domain. To test this postulate, Sprague‐Dawley rats were randomly assigned to one of three experimental groups: control, 6‐, or 12‐hour MV. Following 12‐hours of MV, Type I and Type IIa diaphragm myofiber cross sectional areas were decreased by 17% and 23%, respectively. Myonuclear content was also decreased after 12‐hours of MV and resulted in the maintenance of a constant myonuclear domain in all fiber types. Both 6‐ and 12‐hour MV resulted in significant increases in the number of terminal deoxynucleotidyl transferase (TdT)‐mediated dUTP nick‐end labeling (TUNEL) positive nuclei in diaphragm fibers. Collectively, these data support the concept that the myonuclear domain of diaphragm myofibers is maintained during MV‐induced atrophy and that myonuclear apoptosis contributes to this maintenance. This work was supported by National Institutes of Health (R01 HL62361).