کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10847662 | 1070363 | 2015 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
24(S)-Hydroxycholesterol induces RIPK1-dependent but MLKL-independent cell death in the absence of caspase-8
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کلمات کلیدی
NF-κBnecrosulfonamide24S-OHC24(S)-HydroxycholesterolCYP46A1MLKLnecrostatin-1TNFRNSAAcyl-CoA:cholesterol acyltransferase 1ACAT1TNFα24S-hydroxycholesterol - 24S-hydroxycholsterolcIAP - ciapNec-1 - NEC-1Alzheimer’s disease - بیماری آلزایمرParkinson’s disease - بیماری پارکینسونtumor necrosis factor α - تومور نکروز عامل αRIPK - ریپکlactate dehydrogenase - لاکتات دهیدروژناز LDH - لاکتات دهیدروژناز به صورت مختصر شده LDH mixed lineage kinase domain-like - مخلوط رده کیناز مانند دامنهCell death - مرگ سلولی cellular inhibitor of apoptosis protein - مهارکننده سلولی پروتئین آپوپتوزNecroptosis - نئروپتوزیسreceptor-interacting protein kinase 1 - پروتئین کیناز 1 گیرنده گیرندهreceptor-interacting protein kinase - پروتئین کیناز گیرنده گیرندهCholesterol 24-hydroxylase - کلسترول 24-هیدروکسیلازtumor necrosis factor receptor - گیرنده فاکتور نکروز تومور
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
24(S)-Hydroxycholesterol (24S-OHC), which is enzymatically produced in the brain, is known to play an important role in maintaining brain cholesterol homeostasis. We have previously reported that 24S-OHC induces a type of non-apoptotic programmed necrosis in neuronal cells expressing little caspase-8. Necroptosis has been characterized as a type of programmed necrosis in which activation of receptor-interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like (MLKL) is involved in the signaling pathway. In the present study, we investigated the involvement of these three proteins in 24S-OHC-induced cell death. We found that RIPK1 but neither RIPK3 nor MLKL was expressed in human neuroblastoma SH-SY5Y cells, while all three proteins were expressed in human T lymphoma caspase-8-deficient Jurkat (JurkatCas8â/â) cells. In JurkatCas8â/â cells, tumor necrosis factor α (TNFα)-induced cell death was significantly suppressed by treatment with respective inhibitors of RIPK1, RIPK3, and MLKL. In contrast, only RIPK1 inhibitor showed significant suppression of 24S-OHC-induced cell death, and even this was less prominent than was observed in TNFα-induced cell death. In JurkatCas8â/â cells, knockdown of either RIPK1 or RIPK3 caused moderate but significant suppression of 24S-OHC-induced cell death, but no such effect was observed as a result of knockdown of MLKL. Collectively, these results suggest that, for both SH-SY5Y cells and JurkatCas8â/â cells, 24S-OHC-induced cell death is dependent on RIPK1 but not on MLKL. We therefore conclude that, in the absence of caspase-8 activity, 24S-OHC induces a necroptosis-like cell death which is RIPK1-dependent but MLKL-independent.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Steroids - Volume 99, Part B, July 2015, Pages 230-237
Journal: Steroids - Volume 99, Part B, July 2015, Pages 230-237
نویسندگان
Diep-Khanh Ho Vo, Yasuomi Urano, Wakako Takabe, Yoshiro Saito, Noriko Noguchi,