FGF-2 and FGF-16 Protect Isolated Perfused Mouse Hearts from Acute Doxorubicin-Induced Contractile Dysfunction
| العنوان: | FGF-2 and FGF-16 Protect Isolated Perfused Mouse Hearts from Acute Doxorubicin-Induced Contractile Dysfunction |
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| المؤلفون: | Peter A. Cattini, Jie Wang, Elissavet Kardami, David P. Sontag |
| المصدر: | Cardiovascular Toxicology. 13:244-253 |
| بيانات النشر: | Springer Science and Business Media LLC, 2013. |
| سنة النشر: | 2013 |
| مصطلحات موضوعية: | Inotrope, medicine.medical_specialty, Cardiotonic Agents, Heart Diseases, Blood Pressure, Myocardial Reperfusion Injury, In Vitro Techniques, Biology, Toxicology, Fibroblast growth factor, Ventricular Function, Left, Mice, chemistry.chemical_compound, Coronary Circulation, Internal medicine, Lactate dehydrogenase, medicine, Animals, Doxorubicin, Molecular Biology, Protein Kinase C, Protein kinase C, Cardioprotection, Antibiotics, Antineoplastic, L-Lactate Dehydrogenase, Myocardial Contraction, Recombinant Proteins, Enzyme Activation, Fibroblast Growth Factors, Endocrinology, Chelerythrine, chemistry, Reperfusion Injury, Fibroblast Growth Factor 2, Cardiology and Cardiovascular Medicine, Anti-Arrhythmia Agents, medicine.drug |
| الوصف: | The anti-cancer drug doxorubicin is associated with an increased risk of cardiac damage and dysfunction, which can be acute as well as chronic. Fibroblast growth factor 2 (FGF-2) provides cardioprotection from ischemia-reperfusion injury but its effects on doxorubicin-induced damage are not known. We investigated the acute effects of doxorubicin administered in the absence and presence of FGF-2 pre-treatment, on isolated mouse perfused heart function over a period of 120 min. Doxorubicin elicited a significant decrease in left ventricular developed pressure (DP) at 30 min that persisted throughout the study. No effect on lactate dehydrogenase levels was detected in the perfusate, suggesting a lack of significant plasma membrane damage. FGF-2 pre-treatment lessened the deleterious effect of doxorubicin on DP significantly, and this beneficial effect of FGF-2 was blunted by protein kinase C inhibition with chelerythrine. Pre-treatment with a non-mitogenic FGF-2 mutant or FGF-16 also protected against a doxorubicin-induced decrease in DP. FGF-16 as well as FGF-2 pre-treatment elicited a small and transient negative inotropic effect. In conclusion, FGF-2 and FGF-16 increase resistance to acute doxorubicin-induced cardiac dysfunction, and protein kinase C activation is implicated in this response. |
| تدمد: | 1559-0259 1530-7905 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::43e8b454a12f67d578eb08f32a91063dTest https://doi.org/10.1007/s12012-013-9203-5Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....43e8b454a12f67d578eb08f32a91063d |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15590259 15307905 |
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