Wilhelm Bloch

Deutsche Sporthochschule Köln, Köln, North Rhine-Westphalia, Germany

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Publications (430)1534.36 Total impact

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  • P Zimmer, W Bloch
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    ABSTRACT: During the last decade, epigenetics became one of the fastest growing research fields in numerous clinical and basic science disciplines. Evidence suggests that chromatin modifications (e.g., histone modifications and DNA methylation) as well as the expression of micro-RNA molecules play a crucial role in the pathogenesis of several cardiovascular diseases. On the one hand, they are involved in the development of general risk factors like chronic inflammation, but on the other hand, epigenetic modifications are conducive to smooth muscle cell, cardiomyocyte, and endothelial progenitor cell proliferation/differentiation as well as to extracellular matrix processing and endothelial function (e.g., endothelial nitric oxide synthase regulation). Therefore, epigenetic medical drugs have gained increased attention and provided the first promising results in the context of cardiovascular malignancies. Beside other lifestyle factors, physical activity and sports essentially contribute to cardiovascular health and regeneration. In this review we focus on recent research proposing physical activity as a potent epigenetic regulator that has the potential to counteract pathophysiological alterations in almost all the aforementioned cardiovascular cells and tissues. As with epigenetic medical drugs, more knowledge about the molecular mechanisms and dose-response relationships of exercise is needed to optimize the outcome of preventive and rehabilitative exercise programs and recommendations.
    Herz 03/2015; DOI:10.1007/s00059-015-4213-7 · 0.78 Impact Factor
  • Philipp Zimmer, Wilhelm Bloch
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    ABSTRACT: During the last decade, epigenetics became one of the fastest growing research fields in numerous clinical and basic science disciplines. Evidence suggests that chromatin modifications (e.g., histone modifications and DNA methylation) as well as the expression of micro-RNA molecules play a crucial role in the pathogenesis of several cardiovascular diseases. On the one hand, they are involved in the development of general risk factors like chronic inflammation, but on the other hand, epigenetic modifications are conducive to smooth muscle cell, cardiomyocyte, and endothelial progenitor cell proliferation/differentiation as well as to extracellular matrix processing and endothelial function (e.g., endothelial nitric oxide synthase regulation). Therefore, epigenetic medical drugs have gained increased attention and provided the first promising results in the context of cardiovascular malignancies. Beside other lifestyle factors, physical activity and sports essentially contribute to cardiovascular health and regeneration. In this review we focus on recent research proposing physical activity as a potent epigenetic regulator that has the potential to counteract pathophysiological alterations in almost all the aforementioned cardiovascular cells and tissues. As with epigenetic medical drugs, more knowledge about the molecular mechanisms and dose-response relationships of exercise is needed to optimize the outcome of preventive and rehabilitative exercise programs and recommendations.
    Herz 03/2015; · 0.91 Impact Factor
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    ABSTRACT: Objectives: The purpose of the present study was to evaluate the effects of superimposed electromyostimulation (E) during cycling on myokines and markers of muscle damage, as E might be a useful tool to induce a high local stimulus to skeletal muscle during endurance training without performing high external workloads. Methods: 13 subjects participated in three experimental trials each lasting 60 min in a randomized order. 1) Cycling (C), 2) Cycling with superimposed E (C+E) and 3) E. Interleukin-6 (IL-6), brain-derived neurotrophic factor (BDNF), creatine kinase (CK) and myoglobin were determined before (pre) and 0', 30', 60', 240' and 24h after each intervention. Results: Only C+E caused significant increases in levels of CK and myoglobin. BDNF and IL-6 significantly increased after C and C+E, however increases for IL-6 were significantly higher after C+E compared to C. Conclusion: The present study showed that superimposed E during cycling might be a useful tool to induce a high local stimulus to skeletal muscle even when performing low to moderate external workloads. This effect might be due the activation of additional muscle fibers and mild eccentric work due to the concomitant activation of agonist and antagonist. However the higher load to skeletal muscle has to be taken into account.
    Journal of musculoskeletal & neuronal interactions 03/2015; 15(1):53-59. · 2.40 Impact Factor
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    ABSTRACT: Improved treatment protocols necessary for survival in pediatric oncology are associated with the development of serious late effects. Of particular importance, especially with regard to physical activity (PA), may be ankle dorsiflexion (DF). This review summarizes the results of observational and exercise intervention studies exploring ankle DF-range of motion (DF-ROM) and/or ankle DF strength in pediatric oncology. PUBMED, Medline, Cochrane library, and SportDiscus were searched by 2 researchers using predefined search terms. The reference lists of included papers and Google scholar were then searched to that ensure all appropriate articles were included. Twelve studies were identified and were observational (n = 8), providing information regarding the status of DF-ROM and/or DF strength, or intervention studies (n = 4) using exercise as a strategy to improve DF function. All observational studies reported some degree of impairment in ankle DF. Two intervention studies found a positive effect of exercise on ankle DF-ROM. The preliminary results suggest that pediatric cancer patients and survivors suffer from limitations in ankle DF with interventions varying in efficacy. It is hoped that this review will enhance the recognition of the limited ankle DF function in pediatric oncology and initiate further research programs focused on targeting and evaluating ankle DF.
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    ABSTRACT: Exercise has been proven to reduce the risk and progression of various diseases, such as cancer, diabetes and neurodegenerative disorders. Increasing evidence suggests that exercise affects the cytokine profile and changes distribution and function of tumor-competitive immune cells. Initial studies have shown that different exercise interventions are associated with epigenetic modifications in different tissues and cell types, such as muscle, fat, brain and blood. The present investigation examines the effect of an intense endurance run (half marathon) on global epigenetic modifications in natural killer (NK) cells in 14 cancer patients compared to 14 healthy controls. We were able to show that histone acetylation and NKG2D expression, a functional NK cell marker, were elevated for at least 24 h after the run. Thus, this is the first study to present a potential mechanism of how exercise may impact NK cell activity on the subcellular level. Further studies should focus on epigenetic mechanisms and dose-dependent effects of exercise. © Georg Thieme Verlag KG Stuttgart · New York.
    International Journal of Sports Medicine 02/2015; DOI:10.1055/s-0034-1398531 · 2.27 Impact Factor
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    ABSTRACT: Chaperone-assisted selective autophagy (CASA) is a tension-induced degradation pathway essential for muscle maintenance. Impairment of CASA causes childhood muscle dystrophy and cardiomyopathy. However, the importance of CASA for muscle function in healthy individuals has remained elusive so far. Here we describe the impact of strength training on CASA in a group of healthy and moderately trained men. We show that strenuous resistance exercise causes an acute induction of CASA in affected muscles to degrade mechanically damaged cytoskeleton proteins. Moreover, repeated resistance exercise during 4 wk of training led to an increased expression of CASA components. In human skeletal muscle, CASA apparently acts as a central adaptation mechanism that responds to acute physical exercise and to repeated mechanical stimulation.
    Autophagy 02/2015; DOI:10.1080/15548627.2015.1017186 · 11.42 Impact Factor
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    ABSTRACT: Mitochondrial dysfunction and alterations in energy metabolism have been implicated in a variety of human diseases. Mitochondrial fusion is essential for maintenance of mitochondrial function and requires the prohibitin ring complex subunit prohibitin-2 (PHB2) at the mitochondrial inner membrane. Here, we provide a link between PHB2 deficiency and hyperactive insulin/IGF-1 signaling. Deletion of PHB2 in podocytes of mice, terminally differentiated cells at the kidney filtration barrier, caused progressive proteinuria, kidney failure, and death of the animals and resulted in hyperphosphorylation of S6 ribosomal protein (S6RP), a known mediator of the mTOR signaling pathway. Inhibition of the insulin/IGF-1 signaling system through genetic deletion of the insulin receptor alone or in combination with the IGF-1 receptor or treatment with rapamycin prevented hyperphosphorylation of S6RP without affecting the mitochondrial structural defect, alleviated renal disease, and delayed the onset of kidney failure in PHB2-deficient animals. Evidently, perturbation of insulin/IGF-1 receptor signaling contributes to tissue damage in mitochondrial disease, which may allow therapeutic intervention against a wide spectrum of diseases. © 2015 The Authors. Published under the terms of the CC BY 4.0 license.
    EMBO Molecular Medicine 02/2015; DOI:10.15252/emmm.201404916 · 8.25 Impact Factor
  • American Journal of Hematology 02/2015; 90(2). DOI:10.1002/ajh.23894 · 3.48 Impact Factor
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    Sebastian Gehlert, Wilhelm Bloch, Frank Suhr
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    ABSTRACT: Abstract: Calcium (Ca2+) plays a pivotal role in almost all cellular processes and ensures the functionality of an organism. In skeletal muscle fibers, Ca2+ is critically involved in the innervation of skeletal muscle fibers that results in the exertion of an action potential along the muscle fiber membrane, the prerequisite for skeletal muscle contraction. Furthermore and among others, Ca2+ regulates also intracellular processes, such as myosin-actin cross bridging, protein synthesis, protein degradation and fiber type shifting by the control of Ca2+-sensitive proteases and transcription factors, as well as mitochondrial adaptations, plasticity and respiration. These data highlight the overwhelming significance of Ca2+ ions for the integrity of skeletal muscle tissue. In this review, we address the major functions of Ca2+ ions in adult muscle but also highlight recent findings of critical Ca2+-dependent mechanisms essential for skeletal muscle-regulation and maintenance.
    International Journal of Molecular Sciences 01/2015; 16(1):1066-1095. DOI:10.3390/ijms16011066 · 2.46 Impact Factor
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    ABSTRACT: The therapeutic impact of exercise interventions in psychiatric diseases such as depression, anxiety and schizophrenia has already been proven through several reviews whereas substance use disorders such as alcohol use disorders (AUD) have so far less frequently been a matter of investigation. Although several publications have summarized studies focusing on physical activities in substance use disorders, no systematic review exists summarizing the evidence of exercise interventions in AUD. A total of 14 studies using the Medline Database, CCMed, Cochrane Library and PsychINFO were identified and met the inclusion criteria. In order to evaluate the evidence, we used the evaluation system of the Oxford Centre for Evidence-Based Medicine (2011). Due to methodological flaws the overall evidence of the studies is rated level "3" but primarily findings confirm that exercise interventions as a complementary treatment component in AUD are feasible and safe. No adverse events were reported. This systematic review indicates that exercise may have beneficial effects on certain domains of physical functioning including VO2max, basal heart rate, physical activity level and strength. Inconsistent effects with a slight trend towards a positive effect on anxiety, mood management, craving, and drinking behavior have been shown and need to be verified. Results must be interpreted cautiously due to the numerous methodological flaws and the heterogeneity of the interventions and measures. However, according to preclinical studies several mechanisms of action are conceivable, especially as to alcohol-related outcomes and additionally seem to be promising. RCTs with high methodological quality are urgently needed in future research to establish evidence-based exercise recommendations for the treatment of AUD. Copyright © 2014 Elsevier Inc. All rights reserved.
  • Nitric Oxide 11/2014; 42C:122-123. DOI:10.1016/j.niox.2014.09.072 · 3.18 Impact Factor
  • Nitric Oxide 11/2014; 42C:123. DOI:10.1016/j.niox.2014.09.073 · 3.18 Impact Factor
  • Nitric oxide : biology and chemistry / official journal of the Nitric Oxide Society; 11/2014
  • Nitric Oxide 11/2014; 42C:123. DOI:10.1016/j.niox.2014.09.074 · 3.18 Impact Factor
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    ABSTRACT: The Nrf2 transcription factor controls the expression of genes involved in the antioxidant defense system. Here, we identified Nrf2 as a novel regulator of desmosomes in the epidermis through the regulation of microRNAs. On Nrf2 activation, expression of miR-29a and miR-29b increases in cultured human keratinocytes and in mouse epidermis. Chromatin immunoprecipitation identified the Mir29ab1 and Mir29b2c genes as direct Nrf2 targets in keratinocytes. While binding of Nrf2 to the Mir29ab1 gene activates expression of miR-29a and -b, the Mir29b2c gene is silenced by DNA methylation. We identified desmocollin-2 (Dsc2) as a major target of Nrf2-induced miR-29s. This is functionally important, since Nrf2 activation in keratinocytes of transgenic mice causes structural alterations of epidermal desmosomes. Furthermore, the overexpression of miR-29a/b or knockdown of Dsc2 impairs the formation of hyper-adhesive desmosomes in keratinocytes, whereas Dsc2 overexpression has the opposite effect. These results demonstrate that a novel Nrf2-miR-29-Dsc2 axis controls desmosome function and cutaneous homeostasis.
    Nature Communications 10/2014; 5:5099. DOI:10.1038/ncomms6099 · 10.74 Impact Factor
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    ABSTRACT: Human red blood cells (RBC) express an active and functional endothelial-like nitric oxide (NO) synthase (RBC-NOS). We report studies on RBC-NOS activity in sickle cell anemia (SCA), a genetic disease characterized by decreased RBC deformability and vascular dysfunction. Total RBC-NOS content was not significantly different in SCA patients compared to healthy controls; however, using phosphorylated RBC-NOS-Ser1177 as a marker, RBC-NOS activation was higher in SCA patients as a consequence of the greater activation of Akt (phosphorylated Akt-Ser473). The higher RBC-NOS activation in SCA led to higher levels of S-nitrosylated α- and β-spectrins, and greater RBC nitrite and nitrotyrosine levels compared to healthy controls. Plasma nitrite content was not different between the two groups. Laser Doppler flowmeter experiments demonstrated blunted microcirculatory NO-dependent response under hyperthermia in SCA patients. RBC deformability, measured by ektacytometry, was reduced in SCA in contrast to healthy individuals, and pre-shearing RBC in vitro did not improve deformability despite an increase of RBC-NOS activation. RBC-NOS activation is high in fresh blood from SCA patients, resulting in high amounts of NO produced by RBC. However, this does not result in improved RBC deformability and vascular function: higher RBC-NO is not sufficient to counterbalance the enhanced oxidative stress in SCA.
    British Journal of Haematology 09/2014; 168(5). DOI:10.1111/bjh.13185 · 4.94 Impact Factor
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    ABSTRACT: Patients suffering from collagen VI related myopathies caused by mutations in COL6A1, COL6A2 and COL6A3 often also display skin abnormalities, like formation of keloids or "cigarette paper" scars, dry skin, striae rubrae and keratosis pilaris (follicular keratosis). Here we evaluated if Col6a1 null mice, an established animal model for the muscle changes in collagen VI related myopathies, are also suitable for the study of mechanisms leading to the skin pathology. We performed a comprehensive study of the expression of all six collagen VI chains in unwounded and challenged skin of wild type and Col6a1 null mice. Expression of collagen VI chains is regulated in both skin wounds and bleomycin-induced fibrosis and the collagen VI α3 chain is proteolytically processed in both wild type and Col6a1 null mice. Interestingly, we detected a decreased tensile strength of the skin and an altered collagen fibril and basement membrane architecture in Col6a1 null mice, the latter being features that are also found in collagen VI myopathy patients. Although Col6a1 null mice do not display an overt wound healing defect, these mice are a relevant animal model to study the skin pathology in collagen VI related disease.
    PLoS ONE 08/2014; 9(8):e105686. DOI:10.1371/journal.pone.0105686 · 3.53 Impact Factor
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    ABSTRACT: Alkylating agents (e.g. sulfur and nitrogen mustards) cause a variety of cell and tissue damage including wound healing disorder. Migration of endothelial cells is of utmost importance for effective wound healing. In this study we investigated the effects of chlorambucil (a nitrogen mustard) on early endothelial cells (EEC) with special focus on cell migration. Chlorambucil significantly inhibited migration of EEC in Boyden chamber and wound healing experiments. Cell migration is linked to cytoskeletal organization. We therefore investigated the distribution pattern of the Golgi apparatus as a marker of cell polarity. Cells are polarized under control conditions, whereas chlorambucil caused an encircling perinuclear position of the Golgi apparatus, indicating non-polarized cells. ROS are discussed to be involved in the pathophysiology of alkylating substances and are linked to cell migration and cell polarity. Therefore we investigated the influence of ROS-scavengers (α-linolenic acid (ALA) and N-acetylcysteine (NAC)) on the impaired EEC migration. Both substances, in particular ALA, improved EEC migration. Notably ALA restored cell polarity. Remarkably, investigations of ROS and RNS biomarkers (8-isoprostane and nitrotyrosine) did not reveal a significant increase after chlorambucil exposure when assessed 24 h post exposure. A distinct breakdown of mitochondrial membrane potential (measured by TMRM) that recovered under ALA treatment was observed. In conclusion our results provide compelling evidence that the alkylating agent chlorambucil dramatically impairs directed cellular migration, which is accompanied by perturbations of cell polarity and mitochondrial membrane potential. ALA treatment was able to reconstitute cell polarity and to stabilize mitochondrial potential resulting in improved cell migration.
    Chemico-Biological Interactions 08/2014; DOI:10.1016/j.cbi.2014.05.015 · 2.98 Impact Factor

Publication Stats

9k Citations
1,534.36 Total Impact Points

Institutions

  • 2005–2015
    • Deutsche Sporthochschule Köln
      • • Abteilung molekulare und zelluläre Sportmedizin
      • • Institut für Kreislaufforschung und Sportmedizin
      Köln, North Rhine-Westphalia, Germany
    • Shandong Cancer Hospital (Shandong Provincial Institute of Cancer Prevention and Treatment)
      Chi-nan-shih, Shandong Sheng, China
  • 2005–2012
    • Heinrich-Heine-Universität Düsseldorf
      Düsseldorf, North Rhine-Westphalia, Germany
  • 1994–2009
    • University of Cologne
      • • Center for Experimental Medicine
      • • Department of Paedatric Cardiology
      • • Department of Cardiothoracic Surgery
      • • Institute of Anatomy I
      Köln, North Rhine-Westphalia, Germany
  • 2002–2008
    • University of Bonn
      • Institut für Physiologie I
      Bonn, North Rhine-Westphalia, Germany
    • University of Münster
      Muenster, North Rhine-Westphalia, Germany
  • 2007
    • University of Freiburg
      Freiburg, Baden-Württemberg, Germany
  • 2006
    • Universitätsklinikum Münster
      Muenster, North Rhine-Westphalia, Germany
    • Universität Ulm
      Ulm, Baden-Württemberg, Germany
  • 2001
    • Lund University
      Lund, Skåne, Sweden
  • 2000
    • Nippon Medical School
      • Department of Otolaryngology
      Tokyo, Tokyo-to, Japan
  • 1999
    • University of Hamburg
      • Department of Neuroanatomy
      Hamburg, Hamburg, Germany
  • 1997
    • MediaPark Klinik Köln
      Köln, North Rhine-Westphalia, Germany