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Modulation of Muscle Derived Cell Survival with N‐acetylcysteine and Dietyl Maleate: Implication for Muscle Cell Based Therapies
Author(s) -
Beckman Sarah Ann,
Drowley Lauren,
Huard Johnny
Publication year - 2010
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.24.1_supplement.lb407
Subject(s) - acetylcysteine , myocyte , oxidative stress , cell , cell therapy , cardiac muscle , skeletal muscle , medicine , cardiac function curve , in vitro , glutathione , cell fusion , pharmacology , heart failure , cancer research , microbiology and biotechnology , antioxidant , chemistry , biology , biochemistry , enzyme
A major issue with cellular transplantation for cardiac repair has been the poor survival of transplanted cells. Cells that have increased survival under stressful conditions could result in improved function. We have previously shown that treating muscle derived stem cells (MDSCs) with antioxidants improves functional cardiac repair, however one of the most abundant cells from skeletal muscle that have been used for cardiac repair is myoblasts. We hypothesize that by altering the level of antioxidants in myoblasts, we will see a similar influence on cell survival and cardiac repair. To examine this, we reduced levels of the antioxidant glutathione with diethyl maleate (DEM) and treated cells with N‐acetylcysteine (NAC), which increases antixoidants. We have examined in vitro characteristics of survival, proliferation, and fusion. Treatment with NAC improved cell survival after oxidative stress compared to DEM and untreated cells. Treatment with DEM decreases fusion compared to NAC and control. Treatment with NAC is simple, inexpensive, and does not cause a permanent transformation of the cells, making this extremely attractive as a potential clinical treatment for cell therapy. This work was supported in part by the Cardiovascular Bioengineering Training Program T‐32 5T32HL076124‐05.