Morphological and functional study of extensor digitorum longus muscle regeneration after iterative crush lesions in mdx mouse

Louboutin, Jean‐Pierre; Fichter‐Gagnepain, Valérie; Pastoret, Christian; Thaon, E.; Noireaud, Jacques; Sebille, Alain; Fardeau, Michel

doi:10.1016/0960-8966(95)00006-9

Cited by 17 publications

(13 citation statements)

References 35 publications

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“…On the other hand, mdx extensor digitorum longus (EDL) muscles showed a return of absolute as well as weight-normalized force to baseline preinjury levels 13 wk after denervation/devascularization-induced injury, whereas these parameters were persistently depressed in the nondystrophic EDL at the same time point (32). Louboutin et al (27) also reported better preservation of weight-normalized tetanic tension in mdx EDL muscles compared with wild type after crush injury. Furthermore, at least in terms of histology alone, most studies have reported that the ability to reconstitute the muscle after massive injury is either equivalent or superior in mdx compared with nondystrophic hindlimb muscles (2,12,21,36,54).…”

Section: Comparison With Previous Studiesmentioning

confidence: 93%

Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury

Matecki

Guibinga

Petrof

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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Section: Comparison With Previous Studiesmentioning

confidence: 93%

Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury

Matecki

Guibinga

Petrof

2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It has been suggested that taurine is a membrane stabilizer. 33,37 Since mdx muscle has a greater capacity for repair than control, 26,38,39 as does the mdx TA compared with DIA, 15,16 the greater amount of taurine in mdx and TA muscles could be a marker of quite a large capacity for muscle regeneration.…”

Section: Growth/dystrophy Studymentioning

confidence: 98%

Nuclear magnetic resonance spectroscopy study of muscle growth,mdx dystrophy and glucocorticoid treatments: correlation with repair

et al. 1998

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“…Skeletal muscle fibers diameters were measured in HE-stained sections of the Quadriceps muscle as previously described. 51 Microdissection and isolation of DNA. Laser microdissected was performed by using Positioning Ablation Laser Micro beam (PALM) (Carl Zeiss, Thornwood, NY, USA).…”

Section: Methodsmentioning

confidence: 99%

Loss of HtrA2/Omi activity in non-neuronal tissues of adult mice causes premature aging

et al. 2012

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mnd2 mice die prematurely as a result of neurodegeneration 30-40 days after birth due to loss of the enzymatic activity of the mitochondrial quality control protease HtrA2/Omi. Here, we show that transgenic expression of human HtrA2/Omi in the central nervous system of mnd2 mice rescues them from neurodegeneration and prevents their premature death. Interestingly, adult transgenic mnd2 mice develop accelerated aging phenotypes, such as premature weight loss, hair loss, reduced fertility, curvature of the spine, heart enlargement, increased autophagy, and death by 12-17 months of age. These mice also have elevated levels of clonally expanded mitochondrial DNA (mtDNA) deletions in their tissues. Our results provide direct genetic evidence linking mitochondrial protein quality control to mtDNA deletions and aging in mammals. Cell Death and Differentiation (2013) 20, 259-269; doi:10.1038/cdd.2012 published online 14 September 2012 Mitochondria are dynamic organelles primarily involved in the production of adenosine triphosphate (ATP) through oxidative phosphorylation. They also play important roles in diverse cellular processes such as cell death, autophagy and innate immunity. 1 As a consequence of oxidative phosphorylation, mitochondria produce reactive oxygen species (ROS), which damages mitochondrial proteins, lipids and nucleic acids, because of their proximity to the source of ROS production. Accumulation over time of mutations and deletions in mitochondrial DNA (mtDNA) together with increased protein misfolding, as a result of ROS damage, leads to ageassociated decline in mitochondrial function, which is believed to be responsible for organismal aging and age-associated diseases. [2][3][4] To maintain optimal mitochondrial function over time, a number of quality control mechanisms exist that monitor and regulate all aspects of mitochondrial physiology. Damaged and unfolded mitochondrial proteins are removed by mitochondrial quality control proteases, which recognize these proteins and degrade them. 5,6 The ATP-dependent AAA (ATPase-Associated with diverse cellular Activities) proteases, are among the best-characterized proteases implicated in mitochondrial protein quality control. 7 The AAA proteases, ClpXP and Lon, located in the matrix are involved in quality control of matrix proteins. Although no specific mitochondrial substrate has been identified for the ClpXP protease, in vitro studies showed that Lon protease preferentially targets oxidatively damaged matrix aconitase. 8 Two additional AAA proteases, Paraplegin (encoded by the SPG7 gene) and YME1L, are associated with the inner membrane with their catalytic sites facing the matrix and intermembrane space, respectively. 7 These proteases are believed to be primarily involved in the degradation of damaged and unfolded membrane proteins of the electron transport chain. In addition, Paraplegin has been shown to process the mitochondrial ribosomal protein MrpL32, 9 suggesting that it might also function in mitochondrial ribosome assembly. Loss-of-functi...

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Morphological and functional study of extensor digitorum longus muscle regeneration after iterative crush lesions in mdx mouse

Cited by 17 publications

References 35 publications

Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury

Regenerative capacity of the dystrophic (mdx) diaphragm after induced injury

Nuclear magnetic resonance spectroscopy study of muscle growth,mdx dystrophy and glucocorticoid treatments: correlation with repair

Loss of HtrA2/Omi activity in non-neuronal tissues of adult mice causes premature aging

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