Aging increases the susceptibility of skeletal muscle derived satellite cells to apoptosis

Jejurikar, Sameer S.; Henkelman, Erika; Cederna, Paul S.; Marcelo, Cynthia L.; Urbanchek, Melanie G.; Kuzon, William M.

doi:10.1016/j.exger.2006.06.053

Cited by 111 publications

(94 citation statements)

References 41 publications

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“…123). Indeed, apoptosis has been suggested to account for muscle atrophy in many diseases, such as skeletal muscle denervation, immobilization, chronic heart failure, skeletal muscle aging, and muscular dystrophy (Sandri et al, 1998;Libera et al, 1999;Vescovo et al, 2000;Sandri et al, 2001;Pollack et al, 2002;Dirks and Leeuwenburgh, 2002;Siu and Alway, 2005;Machida and Booth, 2005;Jejurikar et al, 2006;Chung and Ng, 2006;Siu and Alway, 2009;Wohlgemuth et al, 2010;Narasimhan et al, 2014). Skeletal muscle abnormalities in PD have been reported to include inflammatory myopathies (Gdynia et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Elevated levels of p53 and active caspase-3 have been reported in many muscular diseases, such as aging skeletal muscle and sarcopenia (Chung and Ng, 2006;Marzetti and Leeuwenburgh, 2006). Moreover, apoptosis has been reported to contribute to the muscle atrophy and loss in muscular diseases (Sandri et al, 1998;Libera et al, 1999;Vescovo et al, 2000;Sandri et al, 2001;Pollack et al, 2002;Dirks and Leeuwenburgh, 2002;Siu and Alway, 2005;Machida and Booth, 2005;Jejurikar et al, 2006;Chung and Ng, 2006;Siu and Alway, 2009;Wohlgemuth et al, 2010;Narasimhan et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Apoptotic Mediators are Upregulated in the Skeletal Muscle of Chronic/Progressive Mouse Model of Parkinson's Disease

Erekat

2015

The Anatomical Record

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Apoptosis has been implicated in the pathogenesis of Parkinson disease (PD). Parkinson disease is characterized by skeletal muscle abnormalities. The aim of this study is to illustrate the impact of PD induction on the expression of apoptotic mediators. Twenty normal albino mice were randomly selected and equally divided in control and PD groups. Chronic Parkinsonism was induced in the PD group using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probenecid (MPTP/p). After that, samples from gastrocnemius muscles were evaluated by immunohistochemistry to examine the expression of p53 and active caspase-3 in the two groups of animals. P53 and active caspase-3 expression was significantly higher in gastrocnemius skeletal muscle in PD mice compared with that in the control mice (P value <0.01). Furthermore, we show PD gastrocnemius muscle atrophy measured by significant reduction (P < 0.01) in the muscle fiber cross-sectional area. Thus, our present data suggest that PD induction increased the expression of the apoptotic mediators p53 and active caspase-3 in gastrocnemius muscle, indicating the induction of apoptosis, which was correlative with gastrocnemius muscle atrophy subsequent to the induction of PD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Apoptotic Mediators are Upregulated in the Skeletal Muscle of Chronic/Progressive Mouse Model of Parkinson's Disease

Erekat

2015

The Anatomical Record

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“…In this context, satellite cells and their response to stress such as oxidative stress are important to mature skeletal muscle performance and function. Of significance for our work, enhanced satellite cell apoptosis has been related to compromised recovery potential in skeletal muscle of aged animals ( Jejurikar & Kuzon 2003, Jejurikar et al 2006.…”

Section: Discussionmentioning

confidence: 99%

Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

Colla¹,

Vasconsuelo²,

Boland³

2012

Journal of Endocrinology

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Abstract17b-Estradiol (E 2 ) protects several non-reproductive tissues from apoptosis, including skeletal muscle. We have shown that E 2 at physiological concentrations prevented apoptosis induced by H 2 O 2 in C2C12 skeletal myoblasts. As we also demonstrated the presence of estrogen receptors in mitochondria, the present work was focused on the effects of E 2 on this organelle. Specifically, we evaluated the actions of E 2 on the mitochondrial permeability transition pore (MPTP) by the calcein-acetoxymethylester/cobalt method using fluorescence microscopy and flow cytometry. Pretreatment with E 2 prevented MPTP opening induced by H 2 O 2 , which preceded loss of mitochondrial membrane potential. In addition, it was observed that H 2 O 2 induced translocation of Bax to mitochondria; however, in the presence of the steroid this effect was abrogated suggesting that members of the Bcl-2 family may be regulated by E 2 to exert an antiapoptotic effect. Moreover, E 2 increased mitochondrial manganese superoxide dismutase protein expression and activity, as part of a mechanism activated by E 2 that improved mitochondrial performance. Our results suggest a role of E 2 in the regulation of apoptosis with a clear action at the mitochondrial level in C2C12 skeletal myoblast cells. Key Words" 17b-estradiol " C2C12 skeletal myoblasts

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“…Age‐related changes in muscle are thought to depend on a number of changes including mitochondrial production of reactive oxygen species (Jackson & McArdle, 2011), changes in muscle niche (Carlson & Conboy, 2007) and intracellular changes, such as changes in gene expression (Jejurikar et al ., 2006). Regeneration of adult skeletal muscle is largely dependent on satellite cell population (Morgan & Partridge, 2003).…”

Section: Introductionmentioning

confidence: 99%

Age‐related changes in miR‐143‐3p:Igfbp5 interactions affect muscle regeneration

et al. 2016

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SummaryA common characteristic of aging is defective regeneration of skeletal muscle. The molecular pathways underlying age‐related decline in muscle regenerative potential remain elusive. microRNAs are novel gene regulators controlling development and homeostasis and the regeneration of most tissues, including skeletal muscle. Here, we use satellite cells and primary myoblasts from mice and humans and an in vitro regeneration model, to show that disrupted expression of microRNA‐143‐3p and its target gene, Igfbp5, plays an important role in muscle regeneration in vitro. We identified miR‐143 as a regulator of the insulin growth factor‐binding protein 5 (Igfbp5) in primary myoblasts and show that the expression of miR‐143 and its target gene is disrupted in satellite cells from old mice. Moreover, we show that downregulation of miR‐143 during aging may act as a compensatory mechanism aiming at improving myogenesis efficiency; however, concomitant upregulation of miR‐143 target gene, Igfbp5, is associated with increased cell senescence, thus affecting myogenesis. Our data demonstrate that dysregulation of miR‐143‐3p:Igfbp5 interactions in satellite cells with age may be responsible for age‐related changes in satellite cell function.

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Aging increases the susceptibility of skeletal muscle derived satellite cells to apoptosis

Cited by 111 publications

References 41 publications

Apoptotic Mediators are Upregulated in the Skeletal Muscle of Chronic/Progressive Mouse Model of Parkinson's Disease

Apoptotic Mediators are Upregulated in the Skeletal Muscle of Chronic/Progressive Mouse Model of Parkinson's Disease

Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

Age‐related changes in miR‐143‐3p:Igfbp5 interactions affect muscle regeneration

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