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  • 1
    Language: English
    In: The Journal of biological chemistry, 04 February 2011, Vol.286(5), pp.3671-80
    Description: The E3 ubiquitin ligase MYCBP2 negatively regulates neuronal growth, synaptogenesis, and synaptic strength. More recently it was shown that MYCBP2 is also involved in receptor and ion channel internalization. We found that mice with a MYCBP2-deficiency in peripheral sensory neurons show prolonged thermal hyperalgesia. Loss of MYCBP2 constitutively activated p38 MAPK and increased expression of several proteins involved in receptor trafficking. Surprisingly, loss of MYCBP2 inhibited internalization of transient receptor potential vanilloid receptor 1 (TRPV1) and prevented desensitization of capsaicin-induced calcium increases. Lack of desensitization, TRPV internalization and prolonged hyperalgesia were reversed by inhibition of p38 MAPK. The effects were TRPV-specific, since neither mustard oil-induced desensitization nor behavioral responses to mechanical stimuli were affected. In summary, we show here for the first time that p38 MAPK activation can inhibit activity-induced ion channel internalization and that MYCBP2 regulates internalization of TRPV1 in peripheral sensory neurons as well as duration of thermal hyperalgesia through p38 MAPK.
    Keywords: Endocytosis ; MAP Kinase Signaling System ; Carrier Proteins -- Physiology ; Trpv Cation Channels -- Metabolism ; P38 Mitogen-Activated Protein Kinases -- Antagonists & Inhibitors
    ISSN: 00219258
    E-ISSN: 1083-351X
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  • 2
    Language: English
    In: Pain, July 2011, Vol.152(7), pp.1455-1458
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.pain.2011.01.042 Byline: Ellen Niederberger, Katharina Kynast, Jorn Lotsch, Gerd Geisslinger Author Affiliation: Pharmazentrum Frankfurt/ZAFES, Institut fur Klinische Pharmakologie, Klinikum der Goethe-Universitat Frankfurt, Frankfurt am Main 60590, Germany Article History: Received 3 December 2010; Revised 19 January 2011; Accepted 21 January 2011 Article Note: (miscellaneous) Sponsorships or completing interests that may be relevant to content are disclosed at the end of this article.
    Keywords: Medicine
    ISSN: 0304-3959
    E-ISSN: 1872-6623
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  • 3
    In: Pain, 2013, Vol.154(3), pp.368-376
    Description: SUMMARY: miRNA-124a is expressed in “pain-relevant” regions of the spinal cord and is regulated during inflammatory nociception. Modulation of miRNA-124a has an impact on the nociceptive response. ABSTRACT: microRNAs (miRNAs) are small noncoding RNAs that have been linked to a number of disease-related signal transduction pathways. Several studies indicate that they are also involved in nociception. It is not clear, however, which miRNAs are important and which genes are modulated by miRNA-associated mechanisms. This study focuses on the regulation and function of the central nervous system (CNS)–specific miRNA-124a in the spinal cord of mice in a formalin model of inflammatory nociception. miRNA-124a is constitutively expressed in the spinal cord of mice, particularly in neurons of the dorsal horn. Peripheral noxious stimulation with formalin led to significant down-regulation of its expression. Knock-down of miRNA-124a by intravenous administration of a specific miRNA-124a inhibitor further increased the nociceptive behavior associated with an upregulation of the pain-relevant miRNA-124a target MeCP2 and proinflammatory marker genes. In contrast, administration of a miRNA-124a mimic counteracted these effects and decreased nociception by down-regulation of the target gene. In conclusion, our results indicate that miRNA-124a is involved in inflammatory nociception by regulation of relevant target proteins and might therefore constitute a novel target for anti-inflammatory therapy.
    Keywords: Inflammation ; Microrna ; Pain ; Spinal Cord ; Target Genes ; Medicine;
    ISSN: 0304-3959
    E-ISSN: 18726623
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  • 4
    Language: English
    In: BMJ: British Medical Journal, 22 June 2013, Vol.346(7913), pp.38-41
    Keywords: Health sciences -- Medical sciences -- Pharmaceutics ; Health sciences -- Medical conditions -- Symptoms ; Health sciences -- Medical sciences -- Pharmacology ; Health sciences -- Medical sciences -- Pharmaceutics ; Health sciences -- Medical sciences -- Pharmaceutics ; Health sciences -- Medical sciences -- Pharmaceutics ; Health sciences -- Medical conditions -- Symptoms ; Health sciences -- Medical treatment -- Drug therapy ; Health sciences -- Medical sciences -- Pharmacology ; Health sciences -- Medical sciences -- Pharmaceutics;
    ISSN: 09598138
    E-ISSN: 17561833
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  • 5
    Language: English
    In: Expert Review of Proteomics, 01 April 2013, Vol.10(2), pp.189-204
    Description: The transcription factor NF-κB was discovered in 1986 and since then has been extensively studied in relation to cancer research and inflammatory or autoimmune diseases due to its important roles in the regulation of apoptosis and inflammation as well as innate and adaptive immunity. Although much is known about NF-κB signaling, novel NF-κB functions in different diseases are still being uncovered, together with its target proteins, interaction partners and regulators of its activation cascade. Proteomic approaches are particularly suited to the discovery of new proteins involved in distinct signal transduction cascades. This review provides an update on and extension of a recent review that summarized a number of proteomic approaches to NF-κB signaling. The studies discussed here utilized innovative techniques and offer several new hypotheses on the role of NF-κB in physiological and pathophysiological processes, which open new avenues for research on NF-κB in the future.
    Keywords: Cancer ; Inflammation ; Nf-Κb ; Proteomics ; Engineering
    ISSN: 1478-9450
    E-ISSN: 1744-8387
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  • 6
    Language: English
    In: PLoS ONE, 2011, Vol.6(12), p.e29240
    Description: Accumulating evidence indicates that increased generation of reactive oxygen species (ROS) contributes to the development of exaggerated pain hypersensitivity during persistent pain. In the present study, we investigated the antinociceptive efficacy of the antioxidants vitamin C and vitamin E in mouse models of inflammatory and neuropathic pain. We show that systemic administration of a combination of vitamins C and E inhibited the early behavioral responses to formalin injection and the neuropathic pain behavior after peripheral nerve injury, but not the inflammatory pain behavior induced by Complete Freund's Adjuvant. In contrast, vitamin C or vitamin E given alone failed to affect the nociceptive behavior in all tested models. The attenuated neuropathic pain behavior induced by the vitamin C and E combination was paralleled by a reduced p38 phosphorylation in the spinal cord and in dorsal root ganglia, and was also observed after intrathecal injection of the vitamins. Moreover, the vitamin C and E combination ameliorated the allodynia induced by an intrathecally delivered ROS donor. Our results suggest that administration of vitamins C and E in combination may exert synergistic antinociceptive effects, and further indicate that ROS essentially contribute to nociceptive processing in special pain states.
    Keywords: Research Article ; Biology ; Medicine ; Neuroscience ; Pharmacology ; Anesthesiology And Pain Management ; Neurological Disorders
    E-ISSN: 1932-6203
    Source: PLoS
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  • 7
    Language: English
    In: Sports Medicine, 2015, Vol.45(11), pp.1497-1509
    Description: Activation of the adenosine monophosphate (AMP)-activated kinase (AMPK) contributes to beneficial effects such as improvement of the hyperglycemic state in diabetes as well as reduction of obesity and inflammatory processes. Furthermore, stimulation of AMPK activity has been associated with increased exercise capacity. A study published in 2008, directly before the Olympic Games in Beijing, showed that the AMPK activator AICAR (5-amino-1-β- d -ribofuranosyl-imidazole-4-carboxamide) increased the running capacity of mice without any training and thus, prompted the World Anti-Doping Agency (WADA) to include certain AMPK activators in the list of forbidden drugs. This raises the question as to whether all AMPK activators should be considered for registration or whether the increase in exercise performance is only associated with specific AMPK-activating substances. In this review, we intend to shed light on currently published AMPK-activating drugs, their working mechanisms, and their impact on body fitness.
    Keywords: Amp-Activated Protein Kinases -- Metabolism ; Exercise Tolerance -- Physiology;
    ISSN: 0112-1642
    E-ISSN: 1179-2035
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  • 8
    Language: English
    In: Sports Medicine, 2015, Vol.45(11), p.1497(13)
    Keywords: Adenosine Monophosphate – Usage ; Hyperglycemia – Prevention ; Obesity – Influence ; Exercise – Usage
    ISSN: 0112-1642
    Source: Cengage Learning, Inc.
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  • 9
    Language: English
    In: Diabetologia, 2014, Vol.57(5), pp.1067-1077
    Description: Byline: Dmitry Namgaladze (1), Sebastian Lips (1), Thomas J. Leiker (2), Robert C. Murphy (2), Kim Ekroos (3), Nerea Ferreiros (4), Gerd Geisslinger (4), Bernhard Brune (1) Keywords: [beta]-Oxidation; Endoplasmic reticulum stress; Fatty acids; Inflammation; Macrophages Abstract: Aims/hypothesis Saturated fatty acids (SFAs) such as palmitate activate inflammatory pathways and elicit an endoplasmic reticulum (ER) stress response in macrophages, thereby contributing to the development of insulin resistance linked to the metabolic syndrome. This study addressed the question of whether or not mitochondrial fatty acid [beta]-oxidation (FAO) affects macrophage responses to SFA. Methods We modulated the activity of carnitine palmitoyl transferase 1A (CPT1A) in macrophage-differentiated THP-1 monocytic cells using genetic or pharmacological approaches, treated the cells with palmitate and analysed the proinflammatory and ER stress signatures. Results To inhibit FAO, we created THP-1 cells with a stable knockdown (KD) of CPT1A and differentiated them to macrophages. Consequently, in CPT1A-silenced cells FAO was reduced. CPT1A KD in THP-1 macrophages increased proinflammatory signalling, cytokine expression and ER stress responses after palmitate treatment. In addition, in human primary macrophages CPT1A KD elevated palmitate-induced inflammatory gene expression. Pharmacological inhibition of FAO with etomoxir recapitulated the CPT1A KD phenotype. Conversely, overexpression of a malonyl-CoA-insensitive CPT1A M593S mutant reduced inflammatory and ER stress responses to palmitate in THP-1 macrophages. Macrophages with a CPT1A KD accumulated diacylglycerols and triacylglycerols after palmitate treatment, while ceramide accumulation remained unaltered. Moreover, lipidomic analysis of ER phospholipids revealed increased palmitate incorporation into phosphatidylethanolamine and phosphatidylserine classes associated with the CPT1A KD. Conclusions/interpretation Our data indicate that FAO attenuates inflammatory and ER stress responses in SFA-exposed macrophages, suggesting an anti-inflammatory impact of drugs that activate FAO. Author Affiliation: (1) Faculty of Medicine, Institute of Biochemistry I/ZAFES, Goethe University Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany (2) Department of Pharmacology, University of Colorado Denver, Aurora, CO, USA (3) Zora Biosciences Oy, Espoo, Finland (4) pharmazentrum Frankfurt/ZAFES, Institute of Clinical Pharmacology, Goethe University Frankfurt, Frankfurt, Germany Article History: Registration Date: 13/01/2014 Received Date: 25/11/2013 Accepted Date: 02/01/2014 Online Date: 01/02/2014 Article note: Dmitry Namgaladze and Sebastian Lips contributed equally to this study. Electronic supplementary material The online version of this article (doi: 10.1007/s00125-014-3173-4) contains peer-reviewed but unedited supplementary material, which is available to authorised users.
    Keywords: β-Oxidation ; Endoplasmic reticulum stress ; Fatty acids ; Inflammation ; Macrophages
    ISSN: 0012-186X
    E-ISSN: 1432-0428
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  • 10
    Language: English
    In: The Lancet, May 1, 2010, Vol.375(9725), p.1569(9)
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/S0140-6736(10)60354-6 Byline: Achim Schmidtko (a), Jorn Lotsch (a), Rainer Freynhagen (b), Gerd Geisslinger (a) Abstract: Pharmacological management of severe chronic pain is difficult to achieve with currently available analgesic drugs, and remains a large unmet therapeutic need. The synthetic peptide ziconotide has been approved by the US Food and Drug Administration and the European Medicines Agency for intrathecal treatment of patients with severe chronic pain that is refractory to other treatment modalities. Ziconotide is the first member in the new drug class of selective N-type voltage-sensitive calcium-channel blockers. The ziconotide-induced blockade of N-type calcium channels in the spinal cord inhibits release of pain-relevant neurotransmitters from central terminals of primary afferent neurons. By this mechanism, ziconotide can effectively reduce pain. However, ziconotide has a narrow therapeutic window because of substantial CNS side-effects, and thus treatment with ziconotide is appropriate for only a small subset of patients with severe chronic pain. We provide an overview of the benefits and limitations of intrathecal ziconotide treatment and review potential future developments in this new drug class. Author Affiliation: (a) Pharmazentrum Frankfurt/ZAFES, Institut fur Klinische Pharmakologie, Goethe-Universitat, Frankfurt am Main, Germany (b) Zentrum fur Anasthesiologie, Intensivmedizin, Schmerztherapie & Palliativmedizin, Schmerzzentrum am Starnberger See, Benedictus Krankenhaus, Tutzing, Germany
    Keywords: Chronic Pain – Care and Treatment
    ISSN: 0140-6736
    E-ISSN: 1474547X
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