Mitochondrial Dysfunction in Skeletal Muscle of Amyloid Precursor Protein-overexpressing Mice

Boncompagni, Simona; Moussa, Charbel; Levy, Ezra; Pezone, Matthew J.; López, José R.; Protasi, Feliciano; Shtifman, Alexander

doi:10.1074/jbc.m112.359588

Cited by 31 publications

(25 citation statements)

References 45 publications

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“…Inclusions and altered cristae morphology were also found in the skeletal muscle of patients with amyotrophic lateral sclerosis (Boncompagni et al, 2012).…”

Section: Discussionmentioning

confidence: 94%

Effect of Cigarette Smoking on the Structure of Hepatocytes: TEM Study

2016

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. Effect of cigarette smoking on the structure of hepatocytes: TEM Study. Int. J. Morphol., 34(4):1239Morphol., 34(4): -1244Morphol., 34(4): , 2016. SUMMARY:The liver is one of the major organs that is indirectly affected by cigarette smoke. The aim of this project is to define the histologic and ultrastructural changes in normal liver cells after exposing animals to cigarette smoke. Thirty albino rats were exposed to cigarette smoke for 90 days, followed by morphologic examination of their livers under light microscope and electron microscope. The liver cells of cigarette smoke exposed rats showed mild swelling with increased eosinophilia. Ultrastructural examination of these cells demonstrated cytoplasm with highly proliferated and crowded mitochondria. There were many electron dense mitochondria. These mitochondria were pleomorphic in shape compared to mitochondrias of control rats. Also, loss of mitochondrial cristae and widening of the intermembranous space was noticed. It is concluded that smoking exerts cellular damage and oxidative stress on normal liver cells resulting in ultrastructural changes.

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“…Inclusions and altered cristae morphology were also found in the skeletal muscle of patients with amyotrophic lateral sclerosis (Boncompagni et al, 2012).…”

Section: Discussionmentioning

confidence: 94%

Effect of Cigarette Smoking on the Structure of Hepatocytes: TEM Study

2016

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“…In another knock-in mouse model of MH, RyR1(R163C), bioenergetics defects, including elevated [Ca 2+ ] m and ROS, and decreased oxidative phosphorylation have been reported (Giulivi et al, 2011). These results imply that there is a Zhou et al, 2010;Yi et al, 2011) Duchenne muscular dystrophy (dystrophin mutations) Robert et al, 2001a;Shkryl et al, 2009;Bellinger et al, 2009;Millay et al, 2008;Goonasekera et al, 2011 (Chang et al, 2012) Smooth muscle atrophy (CSQ-1 knockout) (Paolini et al, 2007) Aging and/or sarcopenia (RyR1, b-amyloid) Boncompagni et al, 2012) n.d., not determined.…”

Section: Ros As Regulatory Signaling Factors In Cardiac and Skeletal mentioning

confidence: 98%

Interactions between sarco-endoplasmic reticulum and mitochondria in cardiac and skeletal muscle – pivotal roles in Ca2+ and reactive oxygen species signaling

Eisner

Csordás

Hajnóczky

2013

Journal of Cell Science

186

174

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SummaryMitochondria are strategically and dynamically positioned in the cell to spatially coordinate ATP production with energy needs and to allow the local exchange of material with other organelles. Interactions of mitochondria with the sarco-endoplasmic reticulum (SR/ER) have been receiving much attention owing to emerging evidence on the role these sites have in cell signaling, dynamics and biosynthetic pathways. One of the most important physiological and pathophysiological paradigms for SR/ER-mitochondria interactions is in cardiac and skeletal muscle. The contractile activity of these tissues has to be matched by mitochondrial ATP generation that is achieved, at least in part, by propagation of Ca 2+ signals from SR to mitochondria. However, the muscle has a highly ordered structure, providing only limited opportunity for mitochondrial dynamics and interorganellar interactions. This Commentary focuses on the latest advances in the structure, function and disease relevance of the communication between SR/ER and mitochondria in muscle. In particular, we discuss the recent demonstration of SR/ER-mitochondria tethers that are formed by multiple proteins, and local Ca 2+ transfer between SR/ER and mitochondria.

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“…Disruption of normal skeletal muscle function is frequently characterized by aberrant intracellular Ca 2+ handling that in some instances may occur well before the appearance of histopathological and clinical symptoms (21, 22). There are two main aspects of skeletal muscle Ca 2+ handling that may be affected by space radiation.…”

Section: Introductionmentioning

confidence: 99%

Divergent Modification of Low-Dose 56Fe-Particle and Proton Radiation on Skeletal Muscle

Shtifman

Pezone²,

Sasi³

et al. 2013

Radiation Research

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It is unknown whether loss of skeletal muscle mass and function experienced by astronauts during space flight could be augmented by ionizing radiation (IR), such as low-dose high-charge and energy (HZE) particles or low-dose high-energy proton radiation. In the current study adult mice were irradiated whole-body with either a single dose of 15 cGy of 1 GeV/n 56Fe-particle or with a 90 cGy proton of 1 GeV/n proton particles. Both ionizing radiation types caused alterations in the skeletal muscle cytoplasmic Ca2+ ([Ca2+]i) homeostasis. 56Fe-particle irradiation also caused a reduction of depolarization-evoked Ca2+ release from the sarcoplasmic reticulum (SR). The increase in the [Ca2+]i was detected as early as 24 h after 56Fe-particle irradiation, while effects of proton irradiation were only evident at 72 h. In both instances [Ca2+]i returned to baseline at day 7 after irradiation. All 56Fe-particle irradiated samples revealed a significant number of centrally localized nuclei, a histologic manifestation of regenerating muscle, 7 days after irradiation. Neither unirradiated control or proton-irradiated samples exhibited such a phenotype. Protein analysis revealed significant increase in the phosphorylation of Akt, Erk1/2 and rpS6k on day 7 in 56Fe-particle irradiated skeletal muscle, but not proton or unirradiated skeletal muscle, suggesting activation of pro-survival signaling. Our findings suggest that a single low-dose 56Fe-particle or proton exposure is sufficient to affect Ca2+ homeostasis in skeletal muscle. However, only 56Fe-particle irradiation led to the appearance of central nuclei and activation of pro-survival pathways, suggesting an ongoing muscle damage/recovery process.

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Mitochondrial Dysfunction in Skeletal Muscle of Amyloid Precursor Protein-overexpressing Mice

Cited by 31 publications

References 45 publications

Effect of Cigarette Smoking on the Structure of Hepatocytes: TEM Study

Effect of Cigarette Smoking on the Structure of Hepatocytes: TEM Study

Interactions between sarco-endoplasmic reticulum and mitochondria in cardiac and skeletal muscle – pivotal roles in Ca2+ and reactive oxygen species signaling

Divergent Modification of Low-Dose 56Fe-Particle and Proton Radiation on Skeletal Muscle

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