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2014 | 27 | 2 | 88-91
Tytuł artykułu

The influence of proteasome inhibitor on the expression of cardiomyocytes damage markers after incubation with doxorubicin

Treść / Zawartość
Warianty tytułu
Języki publikacji
EN
Abstrakty
EN
The aim of the study was to verify the thesis that the cardiotoxic effects of doxorubicin are connected with activation of the ubiquitin - proteasome pathway followed by protein degradation. The expression of myocardial damage markers - fatty acid binding protein (H-FABP) and brain natriuretic peptide (BNP) was evaluated in rat fetal cardiomyocytes simultaneously treated with doxorubicin and the proteasome inhibitor - bortezomib. The level of H-FABP and BNP protein under the influence of doxorubicin was decreased below the detection threshold with unchanged (H-FABP) or elevated (BNP) mRNA expression level. Against the expectations, the inhibitor of proteasome did not abolish this effect. The observed abnormal expression of BNP and H-FABP protein after doxorubicin treatment makes their diagnostic significance in anthracycline cardiotoxicity questionable.
Słowa kluczowe
EN
Wydawca

Rocznik
Tom
27
Numer
2
Strony
88-91
Opis fizyczny
Daty
wydano
2014-06-01
otrzymano
2014-06-11
zaakceptowano
2014-06-13
online
2014-11-25
Twórcy
  • Independent Medical Biology Unit, Medical University of Lublin, Poland
  • Department of Histology and Embryology, Medical University of Lublin, Poland
  • Department of Pneumology Oncology and Allergology, Medical University of Lublin, Poland
  • IMMUNIQ, Beata Solon-Gogol, Sasiedzka 1, 44-240 Zory, Poland
autor
  • Regional Dental Clinic Independent Public Health Care, Lubartowska 58, Lublin, Poland
  • Department of Pediatric Pulmonology and Rheumatology, Medical University of Lublin, Poland
  • Independent Medical Biology Unit, Medical University of Lublin, Poland
  • Independent Medical Biology Unit, Medical University of Lublin, Poland
Bibliografia
  • 1. Adams J.: Development of the Proteasome Inhibitor PS-341. The Oncologist, 7, 9, 2002.
  • 2. Aihara Y. et al.: Doxorubicin Represses CARP Gene Transcription Through the Generation of Oxidative Stress in Neonatal Rat Cardiac Myocytes: Possible Role of Serine/Threonine Kinase - dependent Pathways. J. Mol. Cell Cardiol., 32, 1401, 2000.
  • 3. Batheja R. et al.: Paradoxical decrease in plasma N-terminal-proBNP (NTproBNP) levels in patients receiving doxorubicin chemotherapy and declining left ventricular ejection fraction. J. Am. Coll. Cardiol., 47, 66A, 2006.
  • 4. Chen S., Garami M., Gardner D. G.: Doxorubicin Selectively Inhibits Brain Versus Atrial Natriuretic Peptide Gene Expression in Cultured Neonatal Rat Myocytes. Hypertension, 34, 1223, 1999.
  • 5. Dudka J.: The role of reactive oxygen and nitrogen species in calcium and iron homeostasis dysregulation in anthracycline cardiotoxicity. Postepy Hig. Med. Dosw, 60, 241, 2006.
  • 6. Dudka J. et al.: The diagnosis of anthracycline-induced cardiac damage and heart failure. Postepy Hig. Med. Dosw , 63, 225, 2009.
  • 7. Hacihanefioglu A., Tarkun P., GonulluE.: Acute severe cardiac failure in a myeloma patient due to proteasome inhibitor bortezomib. Int. J. Hematol., 88, 219, 2008.[WoS]
  • 8. Hedhli N., Depre Ch.: Proteasome inhibitors and cardiac cell growth. Cardiovasc. Res., 85, 321, 2010.[WoS]
  • 9. Korga A. et al.: The redox imbalance and the reduction of contractile protein content in rat hearts administered with L-thyroxine and Doxorubicin. Oxid. Med. Cell Longev., 681367, 2012.[WoS]
  • 10. Liu J. et al.: A therapeutic dose of doxorubicin activates ubiquitinproteasome system-mediated proteolysis by acting on both the ubiquitination apparatus and proteasome. Am. J. Physiol. Heart Circ. Physiol., 295, H2541, 2008.
  • 11. Lyu Y. L. et al.: TopoisomeraseIIb-Mediated DNA Double-Strand Breaks: Implications in Doxorubicin Cardiotoxity and Prevention by Dexrazoxane. Cancer Res., 67, 8839, 2007.
  • 12. Minotti G. et al.: Anthracyclines: Molecular Advances and Pharmacologic Developments in Antitumor Activity and Cardiotoxity. Pharmacol. Rev., 56, 185, 2004.
  • 13. Pichon M. F. et al.: Drug - induced Cardiotoxity Studied by Longitudinal B-Type Natriuretic Peptide Asays and Radionuclide Ventryculography. In Vivo, 19, 567, 2005.
  • 14. Ranek M. J., Wang X.: Activation of the Ubiquitin Proteasome System in Doxorubicin Cardiomyopathy. Curr. Hypertens. Rep., 11, 389, 2009.[WoS]
  • 15. Sayed-Ahmad M. M. et al.: Protection by L-Carnitine Against the Inhibition of Gene Expression of Heart Fatty Acid Binding Protein by Chronic Administration of Doxorubicin. Journal of the Egyptian Nat. Cancer Inst., 4, 275, 2000.
  • 16. Sayed-Ahmed M. M. et al.: Inhibition of gene expression of heart fatty acid binding protein and organic cation/carnitine transporter in doxorubicin cardiomyopathic rat model. Eur. J. Pharmacol., 640, 143, 2010.[WoS]
  • 17. Sun Y. et al.: B-Type Natriuretic Peptide-Induced Cardioprotection against Reperfusion Is Associated with Attenaution of Mitochondrial Permeability Transition. Biol. Pharm. Bull, 32, 1545, 2009.
  • 18. Szuławska A., Czyż M.: Molecular mechanisms of anthracyclines action. Postepy Hig. Med. Dosw., 60, 78, 2006.
  • 19. Tsutsui H., Kinugawa S., Matsushima S.: Oxidative Stress and Mitochondrial DNA Damage in Heart Failure”,Circ. J., Suppl Am, A-31, 2008.
  • 20. Voortman J., GiacconeG.: Severe reversible cardiac failure after bortezomib treatment combined with chemotherapy in a non-small cell lung cancer patient: a case report. BMC Cancer, 6, 129, 2006.[Crossref]
Typ dokumentu
Bibliografia
Identyfikatory
Identyfikator YADDA
bwmeta1.element.-psjd-doi-10_2478_cipms-2014-0020
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