Pathways Responsible for Apoptosis Resulting from Amadori-Induced Oxidative and Nitrosative Stress in Human Mesothelial Cells
| العنوان: | Pathways Responsible for Apoptosis Resulting from Amadori-Induced Oxidative and Nitrosative Stress in Human Mesothelial Cells |
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| المؤلفون: | Carlos F. Sánchez-Ferrer, Julián Nevado, Tania Romacho, Susana Vallejo, Carolina Sánchez-Rodríguez, Leocadio Rodríguez-Mañas, Concepción Peiró, Veronica Azcutia, Nuria Matesanz, Mariam El-Assar |
| المصدر: | American Journal of Nephrology. 34:104-114 |
| بيانات النشر: | S. Karger AG, 2011. |
| سنة النشر: | 2011 |
| مصطلحات موضوعية: | Programmed cell death, Cell type, MAP Kinase Signaling System, Nitrogen, Proto-Oncogene Proteins c-jun, viruses, Apoptosis, Inflammation, Biology, medicine.disease_cause, Epithelium, medicine, Animals, Humans, chemistry.chemical_classification, Reactive oxygen species, Cell Death, L-Lactate Dehydrogenase, Phosphatidylethanolamines, Cytochromes c, Cell biology, body regions, Oxidative Stress, chemistry, Nephrology, Hyperglycemia, Cattle, Glycolipids, medicine.symptom, Signal transduction, Mesothelial Cell, Oxidative stress, Signal Transduction |
| الوصف: | Background: Apoptosis and inflammatory/oxidative stress have been associated with hyperglycemia in human peritoneal mesothelial cells (HPMCs) and other cell types. We and others have highlighted the role of early products of non-enzymatic protein glycation in inducing proinflammatory conditions and increasing apoptotic rates in HPMCs. Loss of HPMCs seems to be a hallmark of complications associated with peritoneal membrane dysfunction. The aim of this work is to elucidate the mechanisms by which Amadori adducts may act upon HPMC apoptosis. Methods: HPMCs isolated from different patients were exposed to different Amadori adducts, i.e. highly glycated hemoglobin (10 nM) and glycated bovine serum albumin (250 µg/ml), to study cell death and several proapoptotic markers by different experimental approaches. Results: Amadori adducts, but not their respective controls, impaired cell proliferation and cell viability by means of apoptosis in a time-dependent manner. They regulated the intrinsic mitochondrial cell death signaling pathway and modulated activation of caspases, Bax, iNOS, p53, NF-ĸB, and mitogen-activated protein kinases (p38 and JNK) through different reactive oxygen and nitrosative species. Conclusions: Our data strongly support the idea that long-term hyperglycemia could act as an inducer of apoptosis in HPMCs through Amadori adducts, involving different oxidative and nitrosative reactive species. |
| تدمد: | 1421-9670 0250-8095 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::11489b60014161d48a9465e3deadd569Test https://doi.org/10.1159/000329107Test |
| حقوق: | CLOSED |
| رقم الانضمام: | edsair.doi.dedup.....11489b60014161d48a9465e3deadd569 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 14219670 02508095 |
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