Glutamine preserves skeletal muscle force during an inflammatory insult

Meador, Benjamin M.; Huey, Kimberly A.

doi:10.1002/mus.21430

Cited by 21 publications

(18 citation statements)

References 58 publications

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“…Additional studies have shown that macrophages require high levels of Gln to successfully produce inflammatory mediators as part of the innate immune response for protection against intracellular pathogens (86). Consistent with this notion, results here show that there is a significant positive association between plasma Gln concentrations and HSP70 transcript levels measured in circulating white blood cells from children with malaria.…”

Section: Disclosuresupporting

confidence: 86%

Reduced Hsp70 and Glutamine in Pediatric Severe Malaria Anemia: Role of hemozoin in Suppressing Hsp70 and NF-κB Activation

Kempaiah

Dokładny

Karim

et al. 2016

Mol Med

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Severe malarial anemia (SMA; hemoglobin [Hb] <5.0 g/dL) is a leading global cause of morbidity and mortality among children residing in Plasmodium falciparum transmission regions. Exploration of molecular pathways through global gene expression profiling revealed that SMA was characterized by decreased HSPA1A, a heat shock protein 70 (Hsp70) coding gene. Hsp70 is a ubiquitous chaperone that regulates nuclear factor-kappa B (NF-κB) signaling and production of proinflammatory cytokines known to be important in malaria pathogenesis (for example, IL-1β, IL-6 and TNF-α). Since the role of host Hsp70 in malaria pathogenesis is unexplored, we investigated Hsp70 and molecular pathways in children with SMA. Validation experiments revealed that leukocytic HSP70 transcripts were reduced in SMA relative to nonsevere malaria, and that intraleukocytic hemozoin (PfHz) was associated with lower HSP70. HSP70 was correlated with reticulocyte production and Hb. Since glutamine (Gln) upregulates Hsp70, modulates NF-κB activation and attenuates overexpression of proinflammatory cytokines, circulating Gln was measured in children with malaria. Reduced Gln was associated with increased risk of developing SMA. Treatment of cultured peripheral blood mononuclear cells (PBMCs) with PfHz caused a time-dependent decrease in Hsp70 transcripts/protein and NF-κB activation. Gln treatment of PBMCs overcame PfHz-induced suppression of HSP70 transcripts/protein, reduced NF-κB activation and suppressed overexpression of IL-1β, IL-6 and TNF-α. These findings demonstrate that SMA is characterized by reduced intraleukocytic HSP70 and circulating Gln, and that PfHz-induced suppression of HSP70 can be reversed by Gln. Thus, Gln supplementation may offer important immunotherapeutic options for futures studies in children with SMA.

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Section: Disclosuresupporting

confidence: 86%

Reduced Hsp70 and Glutamine in Pediatric Severe Malaria Anemia: Role of hemozoin in Suppressing Hsp70 and NF-κB Activation

Kempaiah

Dokładny

Karim

et al. 2016

Mol Med

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“…Hind-limb plantarflexor isometric force-production was measured as previously described by our laboratory (Meador and Huey, 2009). Briefly, mice were anesthetized with a ketamine/xylazine (40/3 mg/ml) cocktail which was administered 0.1 ml per 25 g body weight i.p., and the sciatic nerve was exposed through the popliteal fossa in order to electrically stimulate the nerve and elict contraction of the plantarflexors.…”

Section: Methodsmentioning

confidence: 99%

Effect of HSP25 loss on muscle contractile function and running wheel activity in young and old mice

2013

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Aging is associated with an adverse decline in muscle function, often manifesting as decreased strength and increased muscle fatigability that negatively affects the overall health of the elderly. Heat shock proteins (HSPs), a family of stress inducible proteins known to protect cells from damage, are highly induced in muscle cells following exercise, but both basal and inducible levels decline with age. Utilizing young and old mice lacking HSP25 (Hsp25−/−) we tested the hypothesis that HSP25 is required to maintain normal muscle function and that age related decreases in HSP25 directly contribute to declining muscle function. Running wheel distances over 14 days for young Hsp25−/− mice were significantly lower than for the corresponding Hsp25+/+ genotype (81238 vs. 33956 AUC, respectively). While older groups both ran significantly less than young groups, in aged mice HSP25 loss did not lead to any additional decrease. Significantly lower myofibrillar (contractile) protein levels in young Hsp25−/− vs. Hsp25+/+ (15.7 ± 0.2 vs. 13.4 ± 0.3 mg/mg muscle) mice suggests HSP25 loss was associated with greater muscle breakdown during voluntary wheel running. In vivo, plantarflexor maximal isometric force was significantly decreased in aged vs. young mice, but the loss of HSP25 had no effect on either group. However, plantarflexor fatigability over 10 contractions was significantly higher in young Hsp25−/− vs. Hsp25+/+ mice (59 ± 3 vs. 49 ± 4% of initial force, respectively) but no similar effect of genotype was detected in the older groups. There was no difference in muscle caspase-3 activity between Hsp25−/− and Hsp25+/+ mice, whether young or old, but there was a significant genotype independent increase in activity with age. Overall, the results suggest that the absence of HSP25 primarily contributes to muscle fatigue resistance, rather than maximal force production, and that this effect is most evident in young compared to older mice.

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“…Functional testing was completed to detect post-eccentric exercise injury in WT and ␣ 7Tg mice. Maximal isometric force of the plantarflexors was measured in situ as previously described (21) for each of the following groups: WT basal, ␣7Tg basal, WT 7D PE, and ␣7Tg 7D PE (n ϭ 5/grp). The forcemeasurement apparatus consisted of a servomotor and analog control unit (model 305C-LR, Aurora Scientific, Aurora, ON, Canada), a square-wave stimulator (model 2100, A-M Systems, Carlsborg, WA), and a PC running a customized LabView 8.2 program controlling the servomotor and stimulator.…”

Section: Animalsmentioning

confidence: 99%

The α₇β₁-integrin accelerates fiber hypertrophy and myogenesis following a single bout of eccentric exercise

Lueders

Zou

Huntsman

et al. 2011

American Journal of Physiology-Cell Physiology

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The α(7)β(1)-integrin is a heterodimeric transmembrane protein that adheres to laminin in the extracellular matrix, representing a critical link that maintains structure in skeletal muscle. In addition to preventing exercise-induced skeletal muscle injury, the α(7)-integrin has been proposed to act as an intrinsic mechanosensor, initiating cellular growth in response to mechanical strain. The purpose of this study was to determine the extent to which the α(7)-integrin regulates muscle hypertrophy following eccentric exercise. Wild-type (WT) and α(7)-integrin transgenic (α(7)Tg) mice completed a single bout of downhill running exercise (-20°, 17 m/min, 60 min), and gastrocnemius-soleus complexes were collected 1, 2, 4, and 7 days (D) postexercise (PE). Maximal isometric force was maintained and macrophage accumulation was suppressed in α(7)Tg muscle 1D PE. Mean fiber cross-sectional area was unaltered in WT mice but increased 40% in α(7)Tg mice 7D PE. In addition, a rapid and striking fivefold increase in embryonic myosin heavy chain-positive fibers appeared in α(7)Tg mice 2D PE. Although Pax7-positive satellite cells were increased in α(7)Tg muscle 1D PE, the number of nuclei per myofiber was not altered 7D PE. Phosphorylation of mammalian target of rapamycin (mTOR) was significantly elevated in α(7)Tg 1D PE. This study provides the first demonstration that the presence of the α(7)β(1)-integrin in skeletal muscle increases fiber hypertrophy and new fiber synthesis in the early time course following a single bout of eccentric exercise. Further studies are necessary to elucidate the precise mechanism by which the α(7)-integrin can enhance muscle hypertrophy following exercise.

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Glutamine preserves skeletal muscle force during an inflammatory insult

Cited by 21 publications

References 58 publications

Reduced Hsp70 and Glutamine in Pediatric Severe Malaria Anemia: Role of hemozoin in Suppressing Hsp70 and NF-κB Activation

Reduced Hsp70 and Glutamine in Pediatric Severe Malaria Anemia: Role of hemozoin in Suppressing Hsp70 and NF-κB Activation

Effect of HSP25 loss on muscle contractile function and running wheel activity in young and old mice

The α₇β₁-integrin accelerates fiber hypertrophy and myogenesis following a single bout of eccentric exercise

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Glutamine preserves skeletal muscle force during an inflammatory insult

Cited by 21 publications

References 58 publications

Reduced Hsp70 and Glutamine in Pediatric Severe Malaria Anemia: Role of hemozoin in Suppressing Hsp70 and NF-κB Activation

Reduced Hsp70 and Glutamine in Pediatric Severe Malaria Anemia: Role of hemozoin in Suppressing Hsp70 and NF-κB Activation

Effect of HSP25 loss on muscle contractile function and running wheel activity in young and old mice

The α7β1-integrin accelerates fiber hypertrophy and myogenesis following a single bout of eccentric exercise

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The α₇β₁-integrin accelerates fiber hypertrophy and myogenesis following a single bout of eccentric exercise