Heat shock treatment enhances graft cell survival in skeletal myoblast transplantation to the heart

Graft survival after skeletal myoblast transplantation is affected by various pathological processes caused by environmental stress. Heat shock is known to afford protection of several aspects of cell metabolism and function. We hypothesized that prior heat shock treatment of graft cells would impro...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2000-11, Vol.102 (19), p.216-221
Main Authors: SUZUKI, Ken, SMOLENSKI, Ryszard T, JAYAKUMAR, Jay, MURTUZA, Bari, BRAND, Nigel J, YACOUB, Magdi H
Format: Article
Language:English
Subjects:
Animals
Apoptosis
beta-Galactosidase - analysis
beta-Galactosidase - biosynthesis
beta-Galactosidase - genetics
Biological and medical sciences
Cardiology. Vascular system
Cell Hypoxia - physiology
Cell Line
Cell Survival - physiology
Culture Media, Conditioned - metabolism
Genes, Reporter - genetics
Graft Survival - physiology
Heart
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Heart Transplantation
Heat-Shock Proteins - biosynthesis
Heat-Shock Response - physiology
HSP72 Heat-Shock Proteins
In Vitro Techniques
L-Lactate Dehydrogenase - metabolism
Medical sciences
Muscle, Skeletal - cytology
Muscle, Skeletal - drug effects
Muscle, Skeletal - metabolism
Muscle, Skeletal - transplantation
Myocardium - chemistry
Myocardium - cytology
Oxygen - metabolism
Oxygen - pharmacology
Rats
Rats, Sprague-Dawley
Transfection
Transplantation, Heterotopic
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Summary:Graft survival after skeletal myoblast transplantation is affected by various pathological processes caused by environmental stress. Heat shock is known to afford protection of several aspects of cell metabolism and function. We hypothesized that prior heat shock treatment of graft cells would improve their survival after cell transplantation. L6 rat skeletal myoblasts expressing ss-galactosidase (ss-gal) were subjected to heat shock (42 degrees C, 1 hour). Increased expression of heat shock protein 72 was detected 24 hours later in the heat-shocked cells. After hypoxia-reoxygenation in vitro, lactate dehydrogenase leakage was significantly attenuated in the heat-shocked cells; in addition, the percentage of early apoptosis was lower in this group measured by flow cytometry with annexin V staining. For the in vivo study, 1 x 10(6) heat-shocked (hsCTx) or normal-cultured (CTx) myoblasts were infused into the explanted rat hearts through the coronary artery followed by heterotopic heart transplantation. ss-gal activity was significantly higher in the hsCTx group after cell transplantation, with an estimated 8 x 10(6) surviving cells per heart in the hsCTx group and 5 x 10(6) cells in the CTx group on day 28. Discrete loci of grafted cells were globally observed in the myocardium of the hsCTx and CTx groups, with a higher frequency in the hsCTx group. Surviving myoblasts occasionally differentiated into myotubes and had integrated with the native cardiomyocytes. Heat-shocked skeletal myoblasts demonstrated improved tolerance to hypoxia-reoxygenation insult in vitro and enhanced survival when grafted into the heart. Heat shock treatment could be useful in improving graft cell survival in cell transplantation.
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.102.suppl_3.iii-216