Potential role for Id myogenic repressors in apoptosis  and attenuation of hypertrophy in muscles of aged rats

Alway, Stephen E.; Degens, Hans; Krishnamurthy, Gururaj; Smith, Cheryl A.

doi:10.1152/ajpcell.00598.2001

Cited by 142 publications

(150 citation statements)

References 50 publications

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“…† P<0.05 indicates significant difference from aged (26 month) group. n=4 each group It has been suggested that the mechanisms of agerelated apoptosis may differ in fast-and slow-twitch muscle types [21][22][23]. The data of the present study are consistent with this notion.…”

Section: Discussionsupporting

confidence: 91%

Differential regulation of apoptosis in slow and fast twitch muscles of aged female F344BN rats

Rice

Manne

Gadde

et al. 2015

AGE

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Age-related muscle atrophy is characterized by decreases in muscle mass and is thought be mediated, at least in part, by increases in myocyte apoptosis. Recent data has demonstrated that the degree of muscle loss with aging may differ between males and females while other work has suggested that apoptosis as indicated by DNA fragmentation may be regulated differently in fastand slow-twitch muscles. Herein, we investigate how aging affects the regulation of muscle apoptosis in the fast-twitch extensor digitorum longus (EDL) and slow-twitch soleus muscles of young (6-month), aged (26-month), and very aged (30-month) female Fischer 344/NNiaHSD×Brown Norway/BiNia (F344BN) rats. Tissue sections were stained with hydroethidium for ROS and protein extract was subjected to immunoblotting for assessing apoptotic markers. Our data suggest that decreases in muscle mass were associated with increased DNA fragmentation (TUNEL positive) and increases in reactive oxygen species (ROS) as determined by hydroethidium staining in both the EDL and soleus. Similar to our previous work using aged male animals, we observed that the time course and magnitude of changes in Bax, Bcl-2, caspase-3, caspase-9, and cleavage of α-fodrin protein were regulated differently between muscles. These data suggest that aging in the female F344BN rat is associated with decreases in muscle mass, elevations in ROS level, increased muscle cell DNA fragmentation, and alterations in cell membrane integrity and that apoptotic mechanisms may differ between fiber types.

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Section: Discussionsupporting

confidence: 91%

Differential regulation of apoptosis in slow and fast twitch muscles of aged female F344BN rats

Rice

Manne

Gadde

et al. 2015

AGE

View full text Add to dashboard Cite

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“…This pattern was analogous to that observed for tissue levels of HNE and 3-nitrotyrosine, suggesting that the enhanced oxidative and nitrosative stress might have influenced the mitochondrial content of those proteins (Savory, Rao, Huang, Letada, and Herman 1999;Mishra, Randis, Ashraf, and ivoria-Papadopoulos 2006;Qin, Yan, Patel, Liu, and Dong 2006). However, in contrast to previous studies (Alway et al 2002;Alway et al 2003;Song et al 2006;Chung and Ng 2006), we did not detect an age-related increase in the Bax to Bcl-2 ratio. While this finding may be interpreted as a compensatory action aimed at preventing myonuclei loss, we found a concomitant increase of total mitochondrial content of Bid.…”

Section: Discussionsupporting

confidence: 81%

Age-related activation of mitochondrial caspase-independent apoptotic signaling in rat gastrocnemius muscle

Marzetti

Wohlgemuth

Lees

et al. 2008

Mechanisms of Ageing and Development

154

149

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Mitochondria-mediated apoptosis represents a central process driving age-related muscle loss. However, the temporal relation between mitochondrial apoptotic signaling and sarcopenia as well as the regulation of release of pro-apoptotic factors from the mitochondria has not been elucidated. In this study, we investigated mitochondrial apoptotic signaling in skeletal muscle of rats across a wide age range. We also investigated whether mitochondrial-driven apoptosis was accompanied by changes in the expression of Bcl-2 proteins and components of the mitochondrial permeability transition pore (mPTP). Analyses were performed on gastrocnemius muscle of 8-, 18-, 29-and 37-month-old male Fischer 344 ×Brown Norway rats (9 per group). Muscle weight declined progressively with advancing age, concomitant with increased apoptotic DNA fragmentation. Cytosolic and nuclear levels of apoptosis inducing factor (AIF) and endonuclease G (EndoG) increased in old and senescent animals. In contrast, cytosolic levels of cytochrome c were unchanged with age. Mitochondrial Bcl-2, Bax and Bid increased dramatically in 37-month-old rats, with no changes in the Bax/Bcl-2 ratio in any of the age groups. Finally, expression of cyclophilin D was enhanced at very old age. Our findings indicate that the mitochondrial caspase-independent apoptotic pathway may play a more prominent role in skeletal muscle loss than caspase-mediated apoptosis.

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“…Muscle weakness in the elderly is a major health problem (27,28), and hypertrophy induced by overload is greatly attenuated in older animals (29,30). The number of myonuclei might be a limiting factor (19).…”

Section: Discussionmentioning

confidence: 99%

Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining

Bruusgaard

Johansen

Egner

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

255

283

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Effects of previous strength training can be long-lived, even after prolonged subsequent inactivity, and retraining is facilitated by a previous training episode. Traditionally, such "muscle memory" has been attributed to neural factors in the absence of any identified local memory mechanism in the muscle tissue. We have used in vivo imaging techniques to study live myonuclei belonging to distinct muscle fibers and observe that new myonuclei are added before any major increase in size during overload. The old and newly acquired nuclei are retained during severe atrophy caused by subsequent denervation lasting for a considerable period of the animal's lifespan. The myonuclei seem to be protected from the high apoptotic activity found in inactive muscle tissue. A hypertrophy episode leading to a lasting elevated number of myonuclei retarded disuse atrophy, and the nuclei could serve as a cell biological substrate for such memory. Because the ability to create myonuclei is impaired in the elderly, individuals may benefit from strength training at an early age, and because anabolic steroids facilitate more myonuclei, nuclear permanency may also have implications for exclusion periods after a doping offense. muscle memory | muscle nuclei | muscle atrophy | muscle hypertrophy | apoptosis

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Potential role for Id myogenic repressors in apoptosis and attenuation of hypertrophy in muscles of aged rats

Cited by 142 publications

References 50 publications

Differential regulation of apoptosis in slow and fast twitch muscles of aged female F344BN rats

Differential regulation of apoptosis in slow and fast twitch muscles of aged female F344BN rats

Age-related activation of mitochondrial caspase-independent apoptotic signaling in rat gastrocnemius muscle

Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining

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