کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8998307 | 1115619 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effects of an endothelin B receptor agonist on secretory phospholipase A2-IIA-induced apoptosis in cortical neurons
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
sPLA2-IBMCAω-CgTx-GVIAAβL-type voltage-sensitive calcium channelsPLA2-IIABQ788sPLA2PLA2MTT - MTT[Ca2+]i - [Ca2 +] iω-conotoxin GVIA - ω-کنوتوکسین GVIAω-conotoxin MVIIC - ω-کنوتوکسین MVIICphospholipase A2 - آنزیم فسفولیپاز A2 Arachidonic acid - اسید آراشیدونیکSecretory phospholipase A2 - اسید فسفولیپاز A2endothelin - اندوتلینAlzheimer's disease - بیماری آلزایمرsecretory PLA2 - ترشح PLA2TUNEL - تونلApoptosis - خزان یاختهایCNS - دستگاه عصبی مرکزیStroke - سکته مغزیcentral nervous system - سیستم عصبی مرکزیmiddle cerebral artery - شریان مغزی میانیamyloid β protein - پروتئین β آمیلوئیدprostaglandin - پروستاگلاندینهاETB receptor - گیرنده ETB
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب رفتاری
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Endothelin (ET), a vasoconstrictive peptide, acts as an anti-apoptotic factor, and endothelin receptor B (ETB receptor) is associated with neuronal survival in the brain. Human group IIA secretory phospholipase A2 (sPLA2-IIA) is expressed in the cerebral cortex after brain ischemia and causes neuronal cell death via apoptosis. In primary cultures of rat cortical neurons, we investigated the effects of an ETB receptor agonist, ET-3, on sPLA2-IIA-induced cell death. sPLA2-IIA caused neuronal cell death in a concentration- and time-dependent manner. ET-3 significantly prevented neurons from undergoing sPLA2-IIA-induced cell death. These agonists reversed sPLA2-IIA-induced apoptotic features such as the condensation of chromatin and the fragmentation of DNA. Before cell death, sPLA2-IIA potentiated the influx of Ca2+ into neurons. Blockers of the L-type voltage-dependent calcium channel (L-VSCC) not only suppressed the Ca2+ influx, but also exhibited neuroprotective effects. As well as L-VSCC blockers, ET-3 significantly prevented neurons from sPLA2-IIA-induced Ca2+ influx. An ETB receptor antagonist, BQ788, inhibited the effects of ET-3. The present cortical cultures contained few non-neuronal cells, indicating that the ETB receptor agonist affected the survival of neurons directly, but not indirectly via non-neuronal cells. In conclusion, we demonstrate that the ETB receptor agonist rescues cortical neurons from sPLA2-IIA-induced apoptosis. Furthermore, the present study suggests that the inhibition of L-VSCC contributes to the neuroprotective effects of the ETB receptor agonist.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuropharmacology - Volume 48, Issue 2, February 2005, Pages 291-300
Journal: Neuropharmacology - Volume 48, Issue 2, February 2005, Pages 291-300
نویسندگان
Tatsurou Yagami, Keiichi Ueda, Toshiyuki Sakaeda, Noboru Okamura, Hitoshi Nakazato, Takayuki Kuroda, Satoshi Hata, Gaku Sakaguchi, Naohiro Itoh, Yutaka Hashimoto, Masafumi Fujimoto,