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202 results on '"Munz, Barbara"'

10. Skeletal Muscle MicroRNA Patterns in Response to a Single Bout of Exercise in Females: Biomarkers for Subsequent Training Adaptation?

Author

Grieb, Alexandra, primary, Schmitt, Angelika, additional, Fragasso, Annunziata, additional, Widmann, Manuel, additional, Mattioni Maturana, Felipe, additional, Burgstahler, Christof, additional, Erz, Gunnar, additional, Schellhorn, Philipp, additional, Nieß, Andreas M., additional, and Munz, Barbara, additional

Published
2023
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23. Skeletal muscle effects of two different 10‐week exercise regimens, voluntary wheel running, and forced treadmill running, in mice: A pilot study

Author

Schmitt, Angelika, Herzog, Pascal, Röchner, Franziska, Brändle, Anne‐Lena, Fragasso, Annunziata, and Munz, Barbara

Subjects
Male, Receptors, Steroid, Receptors, Thyroid Hormone, mice, lcsh:QP1-981, Nerve Tissue Proteins, Myostatin, Adaptation, Physiological, lcsh:Physiology, Running, DNA-Binding Proteins, Mice, Inbred C57BL, PPAR gamma, MicroRNAs, Physical Conditioning, Animal, forced treadmill running, Animals, voluntary wheel running, skeletal muscle, Muscle, Skeletal, Original Research
Abstract

Physical activity and exercise induce a complex pattern of adaptation reactions in a broad variety of tissues and organs, particularly the cardiovascular and the musculoskeletal systems. The underlying mechanisms, however, specifically the molecular changes that occur in response to training, are still incompletely understood. Animal models help to systematically elucidate the mechanisms of exercise adaptation. With regard to endurance‐based running exercise in mice, two basic regimens have been established: forced treadmill running (FTR), usually consisting of several sessions per week, and voluntary wheel running (VWR). However, the effects of these two programs on skeletal muscle molecular adaptation patterns have never been directly compared. To address this issue, in a pilot study, we analyzed the effects of two ten‐week training regimens in juvenile, male, C57BL/6 mice: moderate‐intensity forced treadmill running three‐times‐a‐week, employing a protocol that has been widely used in similar studies before, and voluntary wheel running. Our data suggest that there are similarities, but also characteristic differences in the molecular responses of different skeletal muscle species to the two training regimens. In particular, we found that VWR induces a significant fiber type shift toward more type IIX fibers in the slow, oxidative soleus muscle (p = .0053), but not in the other three muscles analyzed. In addition, while training‐induced expression patterns of the two metabolic markers Ppargc1a, encoding Pgc‐1α (peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha) and Nr4a3 (nuclear receptor subfamily 4 group A member 3) were roughly similar, downregulation of the Mstn (myostatin) gene and the “atrogene” Fbox32 could only be observed in response to VWR in specific muscles, such as in the gastrocnemius (p = .0015 for Mstn) and in the tibialis anterior (p = .0053 for Fbox32) muscles, suggesting that molecular adaptation reactions to the two training regimens show distinct characteristics., Forced treadmill and voluntary wheel running have differential effects on mouse skeletal muscle, specifically with regard to expression of exercise‐associated genes and miRNAs. In addition, effects differ significantly between individual muscle types.

Published
2020

27. Effects of the anti-oxidant PDTC in combination with a single bout of treadmill running on murine skeletal muscle

Author

Schmitt, Angelika, Anne-Lena Brändle, Herzog, Pascal, Röchner, Franziska, Fragasso, Annunziata, and Munz, Barbara

Subjects
Inflammation, Male, training adaptation, Proline, exercise, ROS, Antioxidants, anti–oxidants, Mice, Inbred C57BL, Mice, lcsh:Biology (General), Thiocarbamates, Physical Conditioning, Animal, lcsh:Pathology, running, Animals, skeletal muscle, PDTC, Muscle, Skeletal, lcsh:QH301-705.5, Research Articles, lcsh:RB1-214, Research Article
Abstract

Objectives: Skeletal muscle adaptation to physical activity is dependent on various factors. Important signaling mediators are reactive oxygen species (ROS). However, recent research suggests that ROS have both beneficial and deleterious effects on exercise adaptation, dependent on training intensity and training status, so that the question of whether anti-oxidants should be taken in connection with exercise cannot easily be answered. Thus, it is important to gain more insight into the complex roles of ROS in regulating training adaptation. Methods: The effects of ROS inhibition on skeletal muscle training adaptation were analyzed by applying the anti-oxidant PDTC, which is also an inhibitor of the ROS-activated transcription factor nuclear factor kappa B (NFκB), to juvenile mice in connection with a single bout of treadmill running. Results: We found that PDTC inhibits exercise-mediated induction of specific stress- and inflammation-associated genes. Other genes, specifically those encoding metabolic and mitochondrial factors, were affected to a lesser extent and there appeared to be little effect on the microRNA (miR) profile. Discussion: Our data suggest that anti-oxidants regulate distinct sets of adaptation-relevant genes, which might have important implications for the design of exercise-based preventive and therapeutic approaches.

Published
2020
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31. Induction of activin A is essential for the neuroprotective action of basic fibroblast growth factor in vivo

Author

Tretter, Yvonne P., Hertel, Moritz, Munz, Barbara, Bruggencate, Gerrit ten, Werner, Sabine, and Alzheimer, Christian

Abstract

Exogenous application of neurotrophic growth factors has emerged as a new and particularly promising approach not only to promote functional recovery after acute brain injury but also to protect neurons against the immediate effect of the injury. Among the various growth factors and cytokines studied so far, the neuroprotective and neurotrophic profile of basic fibroblast growth factor (bFGF) is the best documented. Using an animal model of acute excitotoxic brain injury, we report here that the neuroprotective action of bFGF, which is now being tested in stroke patients, depends on the induction of activin A, a member of the transforming growth factor-[beta] superfamily. Our evidence for this previously unknown mechanism of action of bFGF is that bFGF strongly enhanced lesion-associated induction of activin A; in the presence of the activin-neutralizing protein follistatin, bFGF was no longer capable of rescuing neurons from excitotoxic death; and recombinant activin A exerted a neuroprotective effect by itself. Our data indicate that the development of substances influencing activin expression or receptor binding should offer new ways to fight neuronal loss in ischemic and traumatic brain injury., Author(s): Yvonne P. Tretter [1]; Moritz Hertel [2, 3]; Barbara Munz [2, 4]; Gerrit ten Bruggencate [1]; Sabine Werner [2, 3]; Christian Alzheimer (corresponding author) [1] Consistent with its neuroprotective [...]

Published
2000
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