کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2166039 | 1091808 | 2012 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
A TRPC1-mediated increase in store-operated Ca2+ entry is required for the proliferation of adult hippocampal neural progenitor cells
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کلمات کلیدی
NPCcanonical transient receptor potentialTuj1ANPCTRPCTRPC1SOCESGZThapsigarginTRPV5-bromo-2′-deoxyuridine - 5-bromo-2'-deoxyuridineBrdU - بروموداکسی اوریدینProliferation - ترویجneural progenitor cell - سلول پیشرو عصبیSOC - سیستم روی یک تراشهsubgranular zone - منطقه غده گرانولیStore-operated Ca2+ entry - ورودی Ca2 + ذخیره شدهStore-operated Ca2+ channel - کانال Ca2 + ذخیره شدهCalcium - کلسیم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Adult hippocampal neurogenesis plays an important role in brain function and neurological diseases. Adult neural progenitor cell (aNPC) proliferation is a critical first step in hippocampal neurogenesis. However, the mechanisms that modulate aNPC proliferation have not been fully identified. Ample evidence has demonstrated that cell proliferation is dependent on the intracellular Ca2+ concentration. We hypothesized that store-operated Ca2+ channels (SOCs), which are ubiquitously expressed in all cell types, participate in aNPC proliferation. We found that store-operated Ca2+ entry (SOCE) was involved in the proliferation of aNPCs and that 2-APB, Gd3+ and SKF96365, antagonists of SOCE and canonical transient receptor potential (TRPC), respectively, inhibited the increase in SOCE and aNPC proliferation. We therefore analyzed the expression of TRPCs in aNPCs and showed that TRPC1 is the most significantly upregulated member under proliferative conditions. Interestingly, knockdown of TRPC1 and using an antibody against TRPC1 markedly reduced the degree of SOCE and aNPC proliferation. In parallel, we observed the suppression of aNPC proliferation was found to be associated with cell cycle arrest in G0/G1 phase. Furthermore, gene expression microarray analysis revealed a selective up- or downregulation of 10 genes in aNPCs following TRPC1 silencing. Knockdown of Orai1 or STIM1 also induced a significant inhibition of SOCE and proliferation in aNPCs, and all three proteins were colocalized in the plasma membrane region of cells. Together, these results indicate that SOCE represents a principal mechanism regulating the proliferation of aNPCs and that TRPC1 is an essential component of this pathway. This discovery may be important in improving adult hippocampal neurogenesis and treating cognitive deficits.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Cell Calcium - Volume 51, Issue 6, June 2012, Pages 486-496
Journal: Cell Calcium - Volume 51, Issue 6, June 2012, Pages 486-496
نویسندگان
Maoquan Li, Chunhai Chen, Zhou Zhou, Shangcheng Xu, Zhengping Yu,