دورية أكاديمية
Inhibition of the Na-H + exchanger isoform-1 and the extracellular signal-regulated kinase induces apoptosis: A time course of events
| العنوان: | Inhibition of the Na-H + exchanger isoform-1 and the extracellular signal-regulated kinase induces apoptosis: A time course of events |
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| المؤلفون: | Konstantinidis, D., Koliakos, G., Vafia, K., Liakos, P., Bantekas, C., Trachana, V., Kaloyianni, M. |
| المصدر: | http://www.scopus.com/inward/record.url?eid=2-s2.0-33845697112&partnerID=40&md5=2417177a25b8c6f25460aeac0d7d0079Test. |
| سنة النشر: | 2006 |
| المجموعة: | University of Thessaly Institutional Repository / Ιδρυματικό Αποθετήριο Πανεπιστημίου Θεσσαλίας |
| مصطلحات موضوعية: | Apoptosis, ERK (Extracellular signal-Regulated Kinase), HEp-2 Cell Line, NHE1 (Na +/H + Exchanger Isoform 1), 2 (2 amino 3 methoxyphenyl)chromone, cariporide, caspase 3, DNA fragment, lipocortin 5, mitogen activated protein kinase, reactive oxygen metabolite, sodium proton exchange protein 1, article, atomic absorption spectrometry, cell function, cell pH, DNA synthesis, enzyme activation, enzyme inhibition, enzyme linked immunosorbent assay, HEp 2 cell, human, human cell, priority journal, regulatory mechanism, signal transduction, spectrofluorometry, Annexin A5, Cation Transport Proteins, Cells |
| الوصف: | Aims: The present study attempts to shed light on the role and the relative position of the Na +/H + exchanger isoform 1 (NHE1) and the extracellular signal-regulated kinase (ERK) in HEp-2 cell signaling pathways concerning a diverse range of cellular functions such as regulation of intracellular pH (pHi), DNA synthesis, production of reactive oxygen species (ROS) and apoptosis. Methods: Pharmacological inhibition with cariporide (highly specific inhibitor of NHE1) and PD98059 (specific inhibitor of the upstream activator of ERK) was implemented. Fluorescence spectrometry, atomic absorption spectrometry and ELISA methods were used in order to obtain the results. Results: NHE1 and ERK take part in all of the aforementioned cellular functions, as their inhibition had an effect on all of them. Additionally, inhibition of NHE1 resulted in ERK inhibition as well. Moreover, continuous inhibition of NHE1 or ERK for up to 24h led HEp-2 cells to apoptosis, as assessed through caspase-3 activation, DNA fragmentation and annexin-V binding levels. Conclusion: Our data shows a time course of events in relation to NHE1 and ERK and suggests the existence of a positive feedback loop between NHE1 and ERK which could pose a barrier against apoptosis. Copyright © 2006 S. Karger AG. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | unknown |
| تدمد: | 10158987 |
| العلاقة: | http://hdl.handle.net/11615/29598Test |
| DOI: | 10.1159/000097668 |
| الإتاحة: | https://doi.org/10.1159/000097668Test http://hdl.handle.net/11615/29598Test |
| رقم الانضمام: | edsbas.5F02932D |
| قاعدة البيانات: | BASE |
| تدمد: | 10158987 |
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| DOI: | 10.1159/000097668 |