Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse
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 para...
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2020-05-01
|
| Series: | International Journal of Molecular Sciences |
| Subjects: | |
| Online Access: | https://www.mdpi.com/1422-0067/21/10/3623 |
| _version_ | 1797567450202505216 |
|---|---|
| author | Elena Martínez-Laorden Javier Navarro-Zaragoza María Victoria Milanés María Luisa Laorden Pilar Almela |
| author_facet | Elena Martínez-Laorden Javier Navarro-Zaragoza María Victoria Milanés María Luisa Laorden Pilar Almela |
| author_sort | Elena Martínez-Laorden |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-03-10T19:42:08Z |
| format | Article |
| id | doaj.art-b2e977206c3e42958de93e473ecb6aa5 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T19:42:08Z |
| publishDate | 2020-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-b2e977206c3e42958de93e473ecb6aa52023-11-20T01:10:44ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672020-05-012110362310.3390/ijms21103623Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of AbuseElena Martínez-Laorden0Javier Navarro-Zaragoza1María Victoria Milanés2María Luisa Laorden3Pilar Almela4Department of Pharmacology, Faculty of Medicine, University of Murcia, 30100 Murcia, SpainDepartment of Pharmacology, Faculty of Medicine, University of Murcia, 30100 Murcia, SpainDepartment of Pharmacology, Faculty of Medicine, University of Murcia, 30100 Murcia, SpainDepartment of Pharmacology, Faculty of Medicine, University of Murcia, 30100 Murcia, SpainDepartment of Pharmacology, Faculty of Medicine, University of Murcia, 30100 Murcia, SpainHeat 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.https://www.mdpi.com/1422-0067/21/10/3623heat shock protein 27morphine withdrawalstressheart |
| spellingShingle | Elena Martínez-Laorden Javier Navarro-Zaragoza María Victoria Milanés María Luisa Laorden Pilar Almela Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse International Journal of Molecular Sciences heat shock protein 27 morphine withdrawal stress heart |
| title | Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse |
| title_full | Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse |
| title_fullStr | Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse |
| title_full_unstemmed | Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse |
| title_short | Cardiac Protective Role of Heat Shock Protein 27 in the Stress Induced by Drugs of Abuse |
| title_sort | cardiac protective role of heat shock protein 27 in the stress induced by drugs of abuse |
| topic | heat shock protein 27 morphine withdrawal stress heart |
| url | https://www.mdpi.com/1422-0067/21/10/3623 |
| work_keys_str_mv | AT elenamartinezlaorden cardiacprotectiveroleofheatshockprotein27inthestressinducedbydrugsofabuse AT javiernavarrozaragoza cardiacprotectiveroleofheatshockprotein27inthestressinducedbydrugsofabuse AT mariavictoriamilanes cardiacprotectiveroleofheatshockprotein27inthestressinducedbydrugsofabuse AT marialuisalaorden cardiacprotectiveroleofheatshockprotein27inthestressinducedbydrugsofabuse AT pilaralmela cardiacprotectiveroleofheatshockprotein27inthestressinducedbydrugsofabuse |