Endoplasmic Reticulum Stress is Involved in DFMO Attenuating Isoproterenol-Induced Cardiac Hypertrophy in Rats
العنوان: | Endoplasmic Reticulum Stress is Involved in DFMO Attenuating Isoproterenol-Induced Cardiac Hypertrophy in Rats |
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المؤلفون: | Yan Lin, Jicheng Liu, Jie Lian, Xiaojie Zhang, Bo Li, Wei Xiao, Li Zhou, Jun Wang, Li Jin |
المصدر: | Cellular Physiology and Biochemistry, Vol 38, Iss 4, Pp 1553-1562 (2016) |
بيانات النشر: | Cell Physiol Biochem Press GmbH & Co KG, 2016. |
سنة النشر: | 2016 |
مصطلحات موضوعية: | 0301 basic medicine, Male, Physiology, Cardiac fibrosis, Spermine, Apoptosis, lcsh:Physiology, Muscle hypertrophy, Ornithine decarboxylase, Rats, Sprague-Dawley, chemistry.chemical_compound, 0302 clinical medicine, Polyamines, Myocytes, Cardiac, lcsh:QD415-436, Caspase 12, Heat-Shock Proteins, bcl-2-Associated X Protein, biology, lcsh:QP1-981, Chemistry, Cardiac hypertrophy, 030220 oncology & carcinogenesis, Difluoromethylornithine, Endoplasmic reticulum stress, Atrial Natriuretic Factor, medicine.medical_specialty, Eflornithine, Down-Regulation, Antineoplastic Agents, Cardiomegaly, Ornithine Decarboxylase, Real-Time Polymerase Chain Reaction, lcsh:Biochemistry, 03 medical and health sciences, Bcl-2-associated X protein, Acetyltransferases, Internal medicine, medicine, Animals, Endoplasmic reticulum, Isoproterenol, medicine.disease, Rats, Spermidine, 030104 developmental biology, Endocrinology, biology.protein, Polyamine, Transcription Factor CHOP |
الوصف: | Background/Aims: Studies performed in experimental animals have shown that polyamines contribute to several physiological and pathological processes, including cardiac hypertrophy. This involves an increase in ornithine decarboxylase (ODC) activity and intracellular polyamines associated with regulation of gene expression. Difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, has attracted considerable interest for its antiproliferative role, which it exerts through inhibition of the polyamine pathway and cell turnover. Whether DFMO attenuates cardiac hypertrophy through endoplasmic reticulum stress (ERS) is unclear. Methods: Myocardial hypertrophy was simulated by isoproterenol (ISO). Polyamine depletion was achieved using DFMO. Hypertrophy was estimated using the heart/body index and atrial natriuretic peptide (ANP) gene expression. Cardiac fibrosis and apoptosis were measured by Masson and TUNEL staining. Expression of ODC and spermidine/spermine N1-acetyltransferase (SSAT) were analyzed via real-time PCR and Western blot analysis. Protein expression of ERS and apoptosis factors were analyzed using Western blot analysis. Results: DFMO treatments significantly attenuated hypertrophy and apoptosis induced by ISO in cardiomyocytes. DFMO down-regulated the expression of ODC, glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), cleaved caspase-12, and Bax and up-regulated the expression of SSAT and Bcl-2. Finally, these changes were partially reversed by the addition of exogenous putrescine. Conclusion: The data presented here suggest that polyamine depletion could inhibit cardiac hypertrophy and apoptosis, which is closely related to the ERS pathway. |
اللغة: | English |
تدمد: | 1421-9778 1015-8987 |
الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::40efa923d0652ff144e03f5f3408786fTest http://www.karger.com/Article/FullText/443096Test |
حقوق: | OPEN |
رقم الانضمام: | edsair.doi.dedup.....40efa923d0652ff144e03f5f3408786f |
قاعدة البيانات: | OpenAIRE |
تدمد: | 14219778 10158987 |
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