QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lee, M.-C. Articles by Kim, J.-H. Search for Related Content PubMed PubMed Citation Articles by Lee, M.-C. Articles by Kim, J.-H.

---

Supplement: Nutritional Consequences of Critical Illness Myopathies

Apoptosis of Skeletal Muscle on Steroid-Induced Myopathy in Rats^1,2

Departments of Pathology and ^* Neurosurgery, Chonnam National University Medical School and Research Institute of Medical Science, Gwangju, Korea

³To whom correspondence should be addressed. E-mail: mclee{at}chonnam.ac.kr.

Apoptotic cell death of differentiated skeletal muscle has been reported in an experimental steroid-induced myopathy of rats. To investigate the underlying molecular changes in the apoptosis of skeletal muscle, in situ end labeling (ISEL), Fas expression, and Western blot analysis for apoptosis-related proteins in the soleus muscle of triamcinolone acetonide (TA)-induced myopathy of rats were studied. Proteins for Western blot analysis included Fas-associated death domain (FADD) and caspase 8 for extrinsic pathway, as well as Bcl-2, Bcl-XL, Bax, Bad, Bid, Akt, p-Akt, and caspase 9 for intrinsic pathway. ISEL-positive myonuclei in TA-treated rats were 1.8 ± 1.2%, whereas Fas-positive muscle fibers were 4.5 ± 2.0%. One-fourth of Fas-positive muscle fibers had ISEL-positive myonuclei. Levels of FADD, Bax, Bad, and Bid were substantially increased in the TA-induced myopathy group, whereas Bcl-2, Bcl-XL, Akt, p-Akt, and caspase 9 did not change between control and myopathy groups. Caspase 8 activity increased in the myopathy group. These findings indicate that apoptosis of skeletal muscle in TA-induced myopathy may be triggered by Fas-Fas ligand signals and promoted mainly by overexpression of the pro-apoptotic molecules of FADD and caspase 8 involving the extrinsic pathway. The apoptotic process presented in this study supports a direct, nongenomic effect of a glucocorticoid on cellular membranes leading to cellular apoptosis rather than genomic effector mechanism of steroid hormone mediated by cytosolic steroid receptors.

KEY WORDS: • apoptosis • immunocytochemistry • myopathy • steroid • Western blot

This article has been cited by other articles:

				J. D. Vassallo, E. B. Janovitz, D. M. Wescott, C. Chadwick, L. J. Lowe-Krentz, and L. D. Lehman-McKeeman Biomarkers of Drug-Induced Skeletal Muscle Injury in the Rat: Troponin I and Myoglobin Toxicol. Sci., October 1, 2009; 111(2): 402 - 412. [Abstract] [Full Text] [PDF]

				J. Quadrilatero and J. W. E. Rush Increased DNA fragmentation and altered apoptotic protein levels in skeletal muscle of spontaneously hypertensive rats J Appl Physiol, October 1, 2006; 101(4): 1149 - 1161. [Abstract] [Full Text] [PDF]

				B. W. Tobin and P. N. Uchakin Nutritional Consequences of Critical Illness Myopathies J. Nutr., July 1, 2005; 135(7): 1803S - 1805S. [Full Text] [PDF]