کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9886578 | 1537837 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Role of MEK-ERK pathway in sphingosylphosphorylcholine-induced cell death in human adipose tissue-derived mesenchymal stem cells
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کلمات کلیدی
PBSJnkc-Jun NH2-terminal protein kinaseSPCMSCsGPCRsERKDMSO - DMSOG protein-coupled receptors - G گیرنده های پروتئینی همراهMAPKs - MAPK هاMTT - MTTSphingosylphosphorylcholine - اسپینگزیل فسفرییل کلینAdipose tissue - بافت چربیTUNEL - تونلDimethylsulfoxide - دیمتیل سولفواکسیدMesenchymal stem cell - سلول های بنیادی مزانشیمیMesenchymal stem cells - سلول های بنیادی مزانشیمیHuman adipose tissue-derived mesenchymal stem cells - سلول های بنیادی مزانشیمی مشتق شده از بافت چربی انسانterminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling - مارک نهایی با نام dUTP تخصیص داده شده توسط ترمینال deoxynucleotidyl transferase استPhosphate-buffered saline - محلول نمک فسفات با خاصیت بافریCell death - مرگ سلولی extracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیmitogen-activated protein kinases - کیناز پروتئین فعال Mitogen
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Role of MEK-ERK pathway in sphingosylphosphorylcholine-induced cell death in human adipose tissue-derived mesenchymal stem cells Role of MEK-ERK pathway in sphingosylphosphorylcholine-induced cell death in human adipose tissue-derived mesenchymal stem cells](/preview/png/9886578.png)
چکیده انگلیسی
Sphingosylphosphorylcholine (SPC) is a bioactive lipid molecule involved in a variety of cellular responses. In the present study, we demonstrated that treatment of human adipose tissue-derived mesenchymal stem cells (hATSCs) with d-erythro-SPC resulted in apoptosis-like cell death, as demonstrated by decreased cell viability, DNA strand breaks, the increase of sub-G1 fraction, cytochrome c release into cytosol, and activation of caspase-3. In contrast, the exposure of hATSCs to l-threo-SPC did not induce the cell death, suggesting that the SPC-induced cell death was selective for the d-erythro-stereoisomer of SPC. The d-erythro-SPC-induced cell death was prevented by DEVD-CHO, a caspase-3 specific inhibitor, and Z-VAD-FMK, a general caspase inhibitor, suggesting that the SPC-induced cell death of hATSCs occurs through the cytochrome c- and caspase-3-dependent pathways. In addition, d-erythro-SPC treatment stimulated the activation of mitogen-activated protein kinases, such as ERK and c-Jun NH2-terminal protein kinase (JNK), and the d-erythro-SPC-induced cell death was completely prevented by pretreatment with the MEK inhibitor, U0126, but not by pretreatment with the JNK inhibitor, SP600125, and the p38 MAPK inhibitor, SB202190, suggesting a specific involvement of ERK in the d-erythro-SPC-induced cell death. Pretreatment with U0126 attenuated the d-erythro-SPC-induced release of cytochrome c. From these results, we suggest that ERK is involved in the SPC-induced cell death of hATSC through stimulation of the cytochrome c/caspase-3-dependent pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1734, Issue 1, 1 May 2005, Pages 25-33
Journal: Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids - Volume 1734, Issue 1, 1 May 2005, Pages 25-33
نویسندگان
Eun Su Jeon, Yong Jung Kang, Hae Young Song, Jae Suk Woo, Jin Sup Jung, Yong Keun Kim, Jae Ho Kim,