کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9192134 | 1186615 | 2005 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neurotrophin and GDNF family ligands promote survival and alter excitotoxic vulnerability of neurons derived from murine embryonic stem cells
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کلمات کلیدی
PBSGDNF family ligandLIFGFLESIMHprtNT-4NT-3cytosine arabinosideN-methyl-d-aspartateNMDAAra-C - آرا- CBrdU - بروموداکسی اوریدینbromodeoxyuridine - برومودسوویریدینRET - حقES cells - سلول ESEmbryonic stem cells - سلولهای بنیادی جنینیleukemia inhibitory factor - عامل مهارکننده لوکمیPhosphate buffered saline - فسفات بافر شورMEM - مامانneurturin - نورورتینhypoxanthine guanine phosphoribosyl transferase - هیپوکسانتین گوانین فسفریبوسیل ترانسفرازPersephin - پرسپاینCalcium - کلسیمTrk receptor - گیرنده Trk
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
عصب شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Embryonic stem (ES) cells are genetically manipulable pluripotential cells that can be differentiated in vitro into neurons, oligodendrocytes, and astrocytes. Given their potential utility as a source of replacement cells for the injured nervous system and the likelihood that transplantation interventions might include co-application of growth factors, we examined the effects of neurotrophin and GDNF family ligands on the survival and excitotoxic vulnerability of ES cell-derived neurons (ES neurons) grown in vitro. ES cells were differentiated down a neural lineage in vitro using the 4â/4+ protocol (Bain et al., Dev Biol 168:342-57, 1995). RT-PCR demonstrated expression of receptors for neurotrophins and GDNF family ligands in ES neural lineage cells. Neuronal expression of GFRα1, GFRα2, and ret was confirmed by immunocytochemistry. Exposure to 30-100 ng/ml GDNF or neurturin (NRTN) resulted in activation of ret. Addition of NT-3 and GDNF did not increase cell division but did increase the number of neurons in the cultures 7 days after plating. Pretreatment with NT-3 enhanced the vulnerability of ES neurons to NMDA-induced death (100 μM NMDA for 10 min) and enhanced the NMDA-induced increase in neuronal [Ca2+]i, but did not alter expression of NMDA receptor subunits NR2A or NR2B. In contrast, pretreatment with GDNF reduced the vulnerability of ES neurons to NMDA-induced death while modestly enhancing the NMDA-induced increase in neuronal [Ca2+]i. These findings demonstrate that the response of ES-derived neurons to neurotrophins and GDNF family ligands is largely similar to that of other cultured central neurons.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Neurology - Volume 191, Issue 1, January 2005, Pages 65-76
Journal: Experimental Neurology - Volume 191, Issue 1, January 2005, Pages 65-76
نویسندگان
Chul-Sang Lee, Lee Y. Tee, Susan Dusenbery, Toshihiro Takata, Judith P. Golden, Brian A. Pierchala, David I. Gottlieb, Eugene M. Jr., Dennis W. Choi, B. Joy Snider,