کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8304064 | 1537960 | 2009 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inflammatory protein sPLA2-IIA abrogates TNFα-induced apoptosis in human astroglioma cells: Crucial role of ERK
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کلمات کلیدی
sPLA2-IIAIKBTNFRTNFα receptorERKNF-kBCOX-2FBSJnkDMEMTNFαc-Jun N-terminal kinase - C-Jun N-terminal kinaseDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده Dulbeccotumor necrosis factor α - تومور نکروز عامل αApoptosis - خزان یاختهایfetal bovine serum - سرم جنین گاوAstrocytoma cells - سلولهای استروسیتومCytokines - سیتوکین هاCyclooxygenase-2 - سیکلوکوکسیژناز2tumor necrosis factor - فاکتور نکروز تومورNuclear factor-kB - فاکتور هسته ای kBSecreted phospholipase A2 - فسفولیپاز A2 تثبیت شدهmap - نقشهmitogen-activated protein - پروتئین فعال mitogenprotein kinases - پروتئین کینازextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Brain injury induces the expression of well-known cytokines, such as tumor necrosis factor-alpha (TNFα), and other, which functions are less understood, as secreted phospholipase A2 group IIA (sPLA2-IIA). Since in pathological processes, cytokines function coordinately in networks, to further explore the actions of sPLA2-IIA in tumorigenesis, we investigated the effect of sPLA2-IIA in the presence of TNFα in human 1321N1 astrocytoma cells. In these cells, TNFα activates the apoptotic programme that is accompanied of cytoskeleton changes; however, simultaneous treatment with sPLA2-IIA prevents TNFα-mediated apoptosis and reverses the modification of the markers associated to this response. In fact, the mitogenic activity elicited by the phospholipase alone is preserved. This inhibitory effect is not found in other TNFα-mediated responses, even a functional cooperation is observed on COX-2 protein induction. The cross-talk between TNFα and sPLA2-IIA is associated with ERK activity since its pharmacological inhibition attenuates both synergistic and inhibitory responses. We have also observed that upon sPLA2-IIA stimulation, endogenous ERK has the capacity to bind and phosphorylate sequences present within the cytoplasmic domain of TNFR1/CD120a. These findings thus indicate that sPLA2-IIA and TNFα transduction pathways interact to modulate inflammatory responses and provide additional insights about the capacity of sPLA2-IIA to promote apoptosis resistance in astrocytoma cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1793, Issue 12, December 2009, Pages 1837-1847
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1793, Issue 12, December 2009, Pages 1837-1847
نویسندگان
Elvira Ibeas, LucÃa Fuentes, Rubén MartÃn, Marita Hernández, MarÃa Luisa Nieto,