H9c2 Cardiomyocytes under Hypoxic Stress: Biological Effects Mediated by Sentinel Downstream Targets
| العنوان: | H9c2 Cardiomyocytes under Hypoxic Stress: Biological Effects Mediated by Sentinel Downstream Targets |
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| المؤلفون: | Lucio Quagliuolo, Paola Stiuso, Marina Di Domenico, Giacomo Frati, Luca D'ambrosio, Antonia Feola, Sonia Schiavon, Stefania Lama, Erika Di Zazzo, Giovanni Galasso, Pasqualina Ambrosio, Mariarosaria Boccellino, Daniele Vecchio |
| المساهمون: | Boccellino, Mariarosaria, Galasso, Giovanni, Ambrosio, Pasqualina, Stiuso, Paola, Lama, Stefania, Di Zazzo, Erika, Schiavon, Sonia, Vecchio, Daniele, D’Ambrosio, Luca, Quagliuolo, Lucio, Feola, Antonia, Frati, Giacomo, Domenico Marina, Di, Boccellino, M., Galasso, G., Ambrosio, P., Stiuso, P., Lama, S., Di Zazzo, E., Schiavon, S., Vecchio, D., D'Ambrosio, L., Quagliuolo, L., Feola, A., Frati, G., Di Domenico, M. |
| المصدر: | Oxidative Medicine and Cellular Longevity, Vol 2021 (2021) Oxidative Medicine and Cellular Longevity |
| بيانات النشر: | Hindawi Limited, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | rho GTP-Binding Proteins, Benzylamines, Aging, medicine.medical_specialty, Cell signaling, RHOA, Nitric Oxide Synthase Type III, Article Subject, Cell Survival, MAP Kinase Signaling System, Amidines, Nitric Oxide Synthase Type II, Apoptosis, Biochemistry, Cell Line, Nitric oxide, chemistry.chemical_compound, Skeletal muscle cell differentiation, Downregulation and upregulation, Internal medicine, medicine, Animals, Myocytes, Cardiac, Enzyme Inhibitors, Ventricular remodeling, Cell Proliferation, QH573-671, biology, Cell Biology, General Medicine, Hypoxia (medical), medicine.disease, Cell Hypoxia, Rats, Endothelial stem cell, Oxidative Stress, Glucose, Endocrinology, Proto-Oncogene Proteins c-bcl-2, chemistry, biology.protein, medicine.symptom, Cytology, Research Article |
| الوصف: | The association between diabetes and cardiovascular diseases is well known. Related diabetes macro- and microangiopathies frequently induce hypoxia and consequently energy failure to satisfy the jeopardized myocardium basal needs. Additionally, it is widely accepted that diabetes impairs endothelial nitric oxide synthase (eNOS) activity, resulting in diminished nitric oxide (NO) bioavailability and consequent endothelial cell dysfunction. In this study, we analyzed the embryonic heart-derived H9c2 cell response to hypoxic stress after administration of a high glucose concentration to reproduce a condition often observed in diabetes. We observed that 24 h hypoxia exposure of H9c2 cells reduced cell viability compared to cells grown in normoxic conditions. Cytotoxicity and early apoptosis were increased after exposure to high glucose administration. In addition, hypoxia induced a RhoA upregulation and a Bcl-2 downregulation and lowered the ERK activation observed in normoxia at both glucose concentrations. Furthermore, a significant cell proliferation rate increases after the 1400 W iNOS inhibitor administration was observed. Again, hypoxia increased the expression level of myogenin, a marker of skeletal muscle cell differentiation. The cardiomyocyte gene expression profiles and morphology changes observed in response to pathological stimuli, as hypoxia, could lead to improper ventricular remodeling responsible for heart failure. Therefore, understanding cell signaling events that regulate cardiac response to hypoxia could be useful for the discovery of novel therapeutic approaches able to prevent heart diseases. |
| وصف الملف: | text/xhtml |
| تدمد: | 1942-0994 1942-0900 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::aa6ffe3b1db49b9a609aa3e42339a975Test https://doi.org/10.1155/2021/6874146Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....aa6ffe3b1db49b9a609aa3e42339a975 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19420994 19420900 |
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