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Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse

Department of Pharmacology, Faculty of Medicine, University of Murcia, 30100 Murcia, Spain
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Int. J. Mol. Sci. 2020, 21(10), 3623; https://doi.org/10.3390/ijms21103623
Received: 10 March 2020 / Revised: 16 May 2020 / Accepted: 19 May 2020 / Published: 21 May 2020
Heat shock proteins (HSP) are induced after different stress situations. Some of these proteins, particularly HSP-27, function as markers to indicate cellular stress or damage and protect the heart during addictive processes. Morphine withdrawal induces an enhancement of sympathetic activity in parallel with an increased HSP-27 expression and phosphorylation, indicating a severe situation of stress. HSP-27 can interact with different intracellular signaling pathways. Propranolol and SL-327 were able to antagonize the activation of hypothalamic-pituitary adrenal (HPA) axis and the phosphorylation of HSP-27 observed during morphine withdrawal. Therefore, β-adrenergic receptors and the extracellular signal-regulated kinase (ERK) pathway would be involved in HPA axis activity, and consequently, in HSP-27 activation. Finally, selective blockade of corticotrophin releasing factor (CRF)-1 receptor and the genetic deletion of CRF1 receptors antagonize cardiac adaptive changes. These changes are increased noradrenaline (NA) turnover, HPA axis activation and decreased HSP-27 expression and phosphorylation. This suggests a link between the HPA axis and HSP-27. On the other hand, morphine withdrawal increases µ-calpain expression, which in turn degrades cardiac troponin T (cTnT). This fact, together with a co-localization between cTnT and HSP-27, suggests that this chaperone avoids the degradation of cTnT by µ-calpain, correcting the cardiac contractility abnormalities observed during addictive processes. The aim of our research is to review the possible role of HSP-27 in the cardiac changes observed during morphine withdrawal and to understand the mechanisms implicated in its cardiac protective functions. View Full-Text
Keywords: heat shock protein 27; morphine withdrawal; stress; heart heat shock protein 27; morphine withdrawal; stress; heart
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Martínez-Laorden, E.; Navarro-Zaragoza, J.; Milanés, M.V.; Laorden, M.L.; Almela, P. Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse. Int. J. Mol. Sci. 2020, 21, 3623.

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