کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4326781 | 1614092 | 2010 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Heme oxygenase-1 contributes to pathology associated with thrombin-induced striatal and cortical injury in organotypic slice culture
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کلمات کلیدی
JnkNrf2HO-1ERKc-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKp38 MAPK - P38 MAPKStriatum - استریاتومPar - توسطApoptosis - خزان یاختهایHemorrhagic stroke - سکته هموراژیکNuclear respiratory factor - عامل تنفسی هسته ایMicroglia - میکروگلیاهاheme oxygenase - همگام اکسژنازmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیprotease-activated receptor - گیرنده پروتئاز فعال
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Heme oxygenase-1 contributes to pathology associated with thrombin-induced striatal and cortical injury in organotypic slice culture Heme oxygenase-1 contributes to pathology associated with thrombin-induced striatal and cortical injury in organotypic slice culture](/preview/png/4326781.png)
چکیده انگلیسی
The blood coagulation factor thrombin that leaks from ruptured vessels initiates brain tissue damage after intracerebral hemorrhage. We have recently shown that mitogen-activated protein kinases (MAPKs) activated by thrombin exacerbate hemorrhagic brain injury via supporting survival of neuropathic microglia. Here, we investigated whether induction of heme oxygenase (HO)-1 is involved in these events. Zinc protoporphyrin IX (ZnPP IX), a HO-1 inhibitor, attenuated thrombin-induced injury of cortical cells in a concentration-dependent manner (0.3-3 μM) and tended to inhibit shrinkage of the striatal tissue at 0.3 μM. HO-1 expression was induced by thrombin in microglia and astrocytes in both the cortex and the striatum. The increase of HO-1 protein was suppressed by a p38 MAPK inhibitor SB203580, and early activation of p38 MAPK after thrombin treatment was observed in neurons and microglia in the striatum. Notably, concomitant application of a low concentration (0.3 μM) of ZnPP IX with thrombin induced apoptotic cell death in striatal microglia and significantly decreased the number of activated microglia in the striatal region. On the other hand, a carbon monoxide releaser reversed the protective effect of ZnPP IX on thrombin-induced injury of cortical cells. Overall, these results suggest that p38 MAPK-dependent induction of HO-1 supports survival of striatal microglia during thrombin insults. Thrombin-induced cortical injury may be also regulated by the expression of HO-1 and the resultant production of heme degradation products such as carbon monoxide.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Brain Research - Volume 1347, 6 August 2010, Pages 170-178
Journal: Brain Research - Volume 1347, 6 August 2010, Pages 170-178
نویسندگان
Masatoshi Ohnishi, Hiroshi Katsuki, Kazuhiro Unemura, Yasuhiko Izumi, Toshiaki Kume, Yuki Takada-Takatori, Akinori Akaike,