Marissa K Caldow (Trenerry)

Publications (16) View all

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  Available from: Marissa K Caldow (Trenerry)

  Article: Increased inflammatory cytokine expression in the vastus lateralis of patients with knee osteoarthritis.

  Itamar Levinger, Pazit Levinger, Marissa K Trenerry, Julian A Feller, John R Bartlett, Neil Bergman, Michael J McKenna, David Cameron-Smith
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  ABSTRACT: Increased inflammation and pain are inseparable parts of knee osteoarthritis (OA) that may lead to disuse of the affected limb. The aim of this study was to examine the effects of knee OA on inflammation- and atrophy-related genes and proteins in the vastus lateralis muscle of patients with knee OA. Nineteen patients with knee OA and 14 asymptomatic control subjects matched for age and body mass index underwent strength measurements and a muscle biopsy. Muscle was analyzed for the total cellular protein of inflammatory kinases (p65 NF-κB, JNK1/2, STAT-3, and suppressor of cytokine signaling 3 [SOCS-3]) and inflammatory intracellular molecules (interleukin-6 [IL-6], IL-8, monocyte chemoattractant protein 1 [MCP-1], tumor necrosis factor α [TNFα], IL-1β, and atrogin-1). Knee OA resulted in greater levels of IL-6 protein (34%; P = 0.002). The levels of inflammatory kinases, including STAT-3 (187%; P = 0.002), p65 NF-κB (156%; P = 0.002), and JNK1 (179%; P = 0.027), were also elevated. Furthermore, elevated expression of gene transcripts encoding MCP-1 (28%; P = 0.023), TNFα (85%; P < 0.001), and SOCS-3 (38%; P = 0.055) was observed in patients with knee OA compared with control subjects. Patients with knee OA had reduced muscle strength compared with control subjects (mean ± SEM 84.7 ± 8.7 versus 143.1 ± 20.8 Nm; P = 0.005). Negative correlations were observed between muscle strength and MCP-1 protein abundance (r = -0.37 [P = 0.042]) and the gene expression of TNFα and atrogin-1 messenger RNA (r = -0.46 [P = 0.012] and r = -0.36 [P = 0.040], respectively). Gene expression and the protein abundance of numerous muscle markers of inflammation and atrophy were elevated in patients with knee OA, and the increase in muscle inflammation was associated with a reduction in muscle strength. Given the role inflammation markers may play in muscle strength and atrophy, further studies are needed to investigate the effect of exercise intervention on skeletal muscle inflammation.
  Arthritis & Rheumatism 05/2011; 63(5):1343-8. · 7.87 Impact Factor
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  Available from: Marissa K Caldow (Trenerry)

  Article: Impact of resistance exercise training on interleukin-6 and JAK/STAT in young men.

  Marissa K Trenerry, Paul A Della Gatta, Amy E Larsen, Andrew P Garnham, David Cameron-Smith
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  ABSTRACT: The JAK/STAT signaling pathway is essential for myogenic regeneration and is regulated by a diverse range of ligands, including interleukin-6 (IL-6) and platelet-derived growth factor-BB (PDGF-BB). Our aim was to evaluate the responsiveness of IL-6 and PDGF-BB to intense exercise, along with STAT3 activation, before and after 12 weeks of resistance training. In young men, IL-6 and PDGF-BB protein concentrations were quantified in biopsied muscle and increased at 3 h post-exercise (17.5-fold and 3-fold, respectively). The response was unaltered by 12 weeks of training. Similarly, STAT3 phosphorylation was elevated post-exercise (12.5-fold), irrespective of training status, as was the expression of downstream targets c-MYC (8-fold), c-FOS (4.5-fold), and SOCS3 (2.3-fold). Thus, intense exercise transiently increases IL-6 and PDGF-BB proteins, and STAT3 phosphorylation is increased. These responses are preserved after intense exercise. This suggests they are not modified by training and may be an essential component of the adaptive responses to intense exercise.
  Muscle & Nerve 03/2011; 43(3):385-92. · 2.37 Impact Factor
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  Available from: PubMed Central

  Article: JAK/STAT signaling and human in vitro myogenesis.

  Marissa K Trenerry, Paul A Della Gatta, David Cameron-Smith
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  ABSTRACT: A population of satellite cells exists in skeletal muscle. These cells are thought to be primarily responsible for postnatal muscle growth and injury-induced muscle regeneration. The Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling cascade has a crucial role in regulating myogenesis. In rodent skeletal muscle, STAT3 is essential for satellite cell migration and myogenic differentiation, regulating the expression of myogenic factors. The aim of the present study was to investigate and compare the expression profile of JAK/STAT family members, using cultured primary human skeletal muscle cells. Near confluent proliferating myoblasts were induced to differentiate for 1, 5 or 10 days. During these developmental stages, members of the JAK/STAT family were examined, along with factors known to regulate myogenesis. We demonstrate the phosphorylation of JAK1 and STAT1 only during myoblast proliferation, while JAK2 and STAT3 phosphorylation increases during differentiation. These increases were correlated with the upregulation of genes associated with muscle maturation and hypertrophy. Taken together, these results provide insight into JAK/STAT signaling in human skeletal muscle development, and confirm recent observations in rodents.
  BMC Physiology 03/2011; 11:6.
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  Available from: Marissa K Caldow (Trenerry)

  Article: Repeated sprints alter signaling related to mitochondrial biogenesis in humans.

  Fabio R Serpiello, Michael J McKenna, David J Bishop, Robert J Aughey, Marissa K Caldow, David Cameron-Smith, Nigel K Stepto
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  ABSTRACT: We investigated the effects of acute and chronic repeated-sprint exercise (RSE) on the skeletal muscle messenger RNA (mRNA) expression and protein abundance/phosphorylation associated with mitochondrial biogenesis. Ten healthy young adults (seven males, three females) performed the RSE trial, comprising three sets of 5 × 4-s maximal sprints on a nonmotorized treadmill, with a 20-s recovery between sprints and 4.5 min between sets. After 4 wk of repeated-sprint training, three times per week, participants repeated the RSE. A vastus lateralis muscle biopsy was obtained at rest, immediately after, and 1 and 4 h after RSE, before and after training. Venous blood lactate and glucose were measured at rest and during recovery. Real-time reverse transcriptase polymerase chain reaction and Western blot techniques were used to measure mRNA expression and protein abundance, respectively. Acute RSE increased the phosphorylation of acetyl-CoA carboxylase (86%, effect size (ES) = 1.4 ± 0.8, P < 0.001) and Ca calmodulin-dependent protein kinase II (69%, ES = 0.7 ± 0.6). Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α; 208%, ES = 1.5 ± 0.7, P < 0.001) and nuclear respiratory factor 1 (92%, ES = 0.7 ± 0.8) mRNA expression was increased after RSE. Four weeks of training increased the abundance of PGC-1α protein at rest (33%, ES = 0.9 ± 0.7). Both acute and chronic RSE, despite only 60 s and 12 min of exercise, respectively, altered the molecular signaling associated with mitochondrial adaptations and PGC-1α mRNA expression in skeletal muscle. However, the small-to-moderate changes in resting PGC-1α protein abundance after training, together with the absence of changes in aerobic fitness, require further research to understand the functional significance of PGC-1α in response to RSE.
  Medicine and science in sports and exercise 11/2011; 44(5):827-34. · 3.71 Impact Factor
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  Available from: Marissa K Caldow (Trenerry)

  Article: Impact of SOCS3 overexpression on human skeletal muscle development in vitro.

  Marissa K Caldow, Gregory R Steinberg, David Cameron-Smith
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  ABSTRACT: The Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling cascade has been identified as a crucial factor for myogenesis. The STAT3 isoform is essential for satellite cell migration and myogenic differentiation as it mediates the expression of muscle specific myogenic factors. The SOCS (suppressors of cytokine signaling) family of proteins down-regulates STAT activation. Primary human skeletal muscle cells were isolated and cultured to investigate the effect of SOCS3 adenoviral overexpression on myotube maturation. It was demonstrated that STAT3 inhibition did not influence myotube development or survival. Moreover, SOCS3 overexpression enhances the mRNA expression of downstream targets of STAT3, c-FOS and VEGF. These increases were correlated with enhanced mRNA expression of genes associated with muscle maturation and hypertrophy. Thus SOCS3 influences myoblast differentiation and SOCS3 may be significant in regulating the activity of genes previously identified as transcriptionally regulated by STAT3.
  Cytokine 07/2011; 55(1):104-9. · 3.02 Impact Factor