Sustained Peripheral Arterial Insufficiency Durably Impairs Normal and Regenerating Skeletal Muscle Function

Hourdé, Christophe; Vignaud, Alban; Beurdy, I.; Martelly, Isabelle; Keller, Andreas; Ferry, Arnaud

doi:10.2170/physiolsci.rp008106

Cited by 15 publications

(15 citation statements)

References 29 publications

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“…Cardiotoxin exhibits protein kinase C activity and is a pore-forming agent that causes the degradation of the plasma membrane [8] . In the present study, we verified that hematoxylin-stained transverse sections of myotoxic-treated muscles exhibited centronucleated muscle fibers (regenerating muscle fibers) that filled 1 80-100% of the muscle cross-section area 56 days after myotoxic injury, confirming that our myotoxic treatment resulted in an almost total destruction of tibialis anterior (TA) muscles in every mouse, as previously observed [17,18] . Animals were anesthetized with pentobarbital (60 mg/kg).…”

Section: Myotoxic Treatmentsupporting

confidence: 89%

“…Another explanation of the detrimental effects of diabetes on muscle size may be a decrease in the blood supply to muscles [27] and a deficient neurotransmission [2] . Indeed, efficient muscle vascularization and innervation are known to be essential for muscle maintenance and regeneration [18] . Moreover, both STZ-induced diabetes in Swiss mice and diabetes of genetic origin in Akita mice increased the degree of tetanic fusion of regenerating muscles as well as in uninjured muscles.…”

Section: Discussionmentioning

confidence: 99%

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Diabetes Provides an Unfavorable Environment for Muscle Mass and Function after Muscle Injury in Mice

Vignaud¹,

Ramond²,

Hourdé³

et al. 2007

Pathobiology

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It is of common knowledge that diabetes decreases skeletal muscle contractility and induces atrophy. However, how hyperglycemia and insulin deficiency modify muscle mass and neuromuscular recovery after muscle injury is not well known. We have analyzed two models of diabetes: streptozotocin (STZ)-treated Swiss mice and Akita mice that spontaneously develop diabetes. A fast muscle, the tibialis anterior, was injured following injection of a myotoxic agent (cardiotoxin). Neuromuscular function was evaluated by examining in situ isometric contractile properties of regenerating muscles in response to nerve stimulation 14, 28 and 56 days after myotoxic injury. We found that STZ-induced diabetes reduces muscle weight and absolute maximal tetanic force in both regenerating and uninjured muscles (p = 0.0001). Moreover, it increases specific maximal tetanic force and tetanic fusion in regenerating and uninjured muscles (p = 0.04). In the Akita mice, diabetes decreases muscle weight and absolute maximal tetanic force, and increases tetanic fusion in both regenerating and uninjured muscles (p ≤ 0.003). Interestingly, STZ-induced diabetes exerts more marked effects than diabetes of genetic origin, in particular on muscle weight. This reduction in muscle mass was not due to an increased expression of the atrogenes MuRF1 and atrogin-1 during STZ-induced diabetes. The present study in mice demonstrates that both models of diabetes impair regenerating muscles as well as uninjured muscles. Regenerating fast muscles are weaker, lighter and slower in diabetic compared with nondiabetic mice.

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Section: Myotoxic Treatmentsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Diabetes Provides an Unfavorable Environment for Muscle Mass and Function after Muscle Injury in Mice

Vignaud¹,

Ramond²,

Hourdé³

et al. 2007

Pathobiology

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“…Expression levels of ␤-enolase are at least twofold higher in fast-twitch muscle, which relies on glycolysis compared to slow muscles such as the Soleus, which mostly relies on oxidative energy metabolism (Keller et al, 1995). Thus, ␤-enolase is a good marker of fast-glycolytic fibers (Fougerousse et al, 2001;Hourde et al, 2005Hourde et al, , 2006.…”

Section: Introductionmentioning

confidence: 99%

Novel murine clonal cell lines either express slow or mixed (fast and slow) muscle markers following differentiation in vitro

Peltzer

Colman

Cebrián

et al. 2008

Developmental Dynamics

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We have investigated whether the phenotype of myogenic clones derived from satellite cells of different muscles from the transgenic immortomouse depended on muscle type origin. Clones derived from neonatal, or 6-to 12-week-old fast and slow muscles, were analyzed for myosin and enolase isoforms as phenotypic markers. All clones derived from slow-oxidative muscles differentiated into myotubes with a preferentially slow contractile phenotype, whereas some clones derived from rapid-glycolytic or neonatal muscles expressed both fast and slow myosin isoforms. Thus, muscle origin appears to bias myosin isoform expression in myotubes. The neonatal clone (WTt) was cultivated in various medium and substrate conditions, allowing us to determine optimized conditions for their differentiation. Matrigel allowed expressions of adult myosin isoforms, and an isozymic switch from embryonic ␣-toward muscle-specific ␤-enolase, never previously observed in vitro. These cells will be a useful model for in vitro studies of muscle fiber maturation and plasticity.

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“…Blood supply is also considered to play an important role in muscle repair [11,12]. This was recently confirmed by a study reporting that arterial peripheral insufficiency decreased muscle recovery after injury [19]. We therefore hypothesised that the reduced blood supply due to microvascular leakage observed after IR [1] explains the reduced muscle recovery after IR injury.…”

Section: Discussionmentioning

confidence: 81%

“…It has been previously documented that a reduced blood supply impairs muscle recovery following injury [19]. To test the hypothesis that a reduction in muscle blood supply could explain the difference between ischemic/reperfused and myotoxin-treated muscles, we also analysed muscle capillarity.…”

Section: Further Analysis Of Injured Musclesmentioning

confidence: 99%

The Effect of Two-Week Resistance and Endurance Training on Skeletal Muscle Repair and Regeneration after Ischemia-Reperfusion in Rat

Lim¹,

Kim²

2017

Exerc Sci

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Ischemia/reperfusion (IR) injury can induce skeletal muscle fibre death and subsequent regeneration. By 14 days, absolute and specific maximal forces and fatigue resistance in ischemic/reperfused soleus muscles were still reduced (−89%, −81%, and −75%, resp.) as compared to control muscles (P < .05). The decrease of these parameters in ischemic/reperfused muscle was much greater than that of myotoxic injured muscles (−12%, −11%, and −19%; P < .05). In addition, at 14 days ischemic/reperfused muscle structure was still abnormal, showing small muscle fibres expressing neonatal myosin heavy chain and large necrotic muscle fibres that were not observed in myotoxin treated muscles. By 56 days, in contrast to myotoxin treated muscles, specific maximal force and muscle weight of the ischemic/reperfused muscles did not fully recover (P < .05). This differential recovery between ischemic/reperfused and myotoxin treated muscles was not related to the differences in the initial cell death, loss of satellite cells after injury, expression of growth factors (IGF1, IGF2..), or capillary density in regenerating muscles. In conclusion, our results demonstrate that IR injury in mice induces long term detrimental effects in skeletal muscles and that the recovery following IR injury was delayed for yet unknown reasons as compared to myotoxic injury.

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Sustained Peripheral Arterial Insufficiency Durably Impairs Normal and Regenerating Skeletal Muscle Function

Cited by 15 publications

References 29 publications

Diabetes Provides an Unfavorable Environment for Muscle Mass and Function after Muscle Injury in Mice

Diabetes Provides an Unfavorable Environment for Muscle Mass and Function after Muscle Injury in Mice

Novel murine clonal cell lines either express slow or mixed (fast and slow) muscle markers following differentiation in vitro

The Effect of Two-Week Resistance and Endurance Training on Skeletal Muscle Repair and Regeneration after Ischemia-Reperfusion in Rat

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