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http://www.ncbi.nlm.nih.gov/pubmed/21087236
1 G' u) p% b( D# KJ Neurosci. 2010 Nov 10;30(45):14931-6.% s: u4 S* R* Y7 k6 S! }! }4 \3 t
% A: a# n5 G, r eMicroRNA regulation of neural stem cells and neurogenesis.' r. Y/ K, L4 ^3 C. V# E
Shi Y, Zhao X, Hsieh J, Wichterle H, Impey S, Banerjee S, Neveu P, Kosik KS., s) R2 S: t" C6 \! u) u9 l. a3 Z
5 y r' G$ e7 b5 l3 n; l6 e0 | cDepartment of Neurosciences, Beckman Research Institute of City of Hope, Duarte, California 91010, USA. yshi@coh.org
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Abstract
4 a. o! Q; L `5 QMicroRNAs are a class of small RNA regulators that are involved in numerous cellular processes, including development, proliferation, differentiation, and plasticity. The emerging concept is that microRNAs play a central role in controlling the balance between stem cell self-renewal and fate determination by regulating the expression of stem cell regulators. This review will highlight recent advances in the regulation of neural stem cell self-renewal and neurogenesis by microRNAs. It will cover microRNA functions during the entire process of neurogenesis, from neural stem cell self-renewal and fate determination to neuronal maturation, synaptic formation, and plasticity. The interplay between microRNAs and both cell-intrinsic and -extrinsic stem cell players, including transcription factors, epigenetic regulators, and extrinsic signaling molecules will be discussed. This is a summary of the topics covered in the mini-symposium on microRNA regulation of neural stem cells and neurogenesis in SFN 2010 and is not meant to be a comprehensive review of the subject.+ J' w8 K7 }: ^; t; B, R
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2.链接
6 A7 T3 Z0 z2 t6 f! z- c thttp://www.ncbi.nlm.nih.gov/pubmed/21051628
7 Y _6 x9 W" zScience. 2010 Nov 5;330(6005):774-8.
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Specification and morphogenesis of astrocytes.- X. g( N$ [8 r2 p( x
Freeman MR.. [- r* o: c, c( q$ A/ B
9 w5 H/ }) v( \" x, o6 w* U% U5 P4 F5 @; TDepartment of Neurobiology, Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester, MA 01605, USA. marc.freeman@umassmed.edu
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' V& [" b; F9 }6 V1 m' T; f+ `Abstract* w0 I% ?& `) `) u0 i7 s: W- @
Astrocytes are the most abundant cell type in the mammalian brain. Interest in astrocyte function has increased dramatically in recent years because of their newly discovered roles in synapse formation, maturation, efficacy, and plasticity. However, our understanding of astrocyte development has lagged behind that of other brain cell types. We do not know the molecular mechanism by which astrocytes are specified, how they grow to assume their complex morphologies, and how they interact with and sculpt developing neuronal circuits. Recent work has provided a basic understanding of how intrinsic and extrinsic mechanisms govern the production of astrocytes from precursor cells and the generation of astrocyte diversity. Moreover, new studies of astrocyte morphology have revealed that mature astrocytes are extraordinarily complex, interact with many thousands of synapses, and tile with other astrocytes to occupy unique spatial domains in the brain. A major challenge for the field is to understand how astrocytes talk to each other, and to neurons, during development to establish appropriate astrocytic and neuronal network architectures.
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3.链接
* v) K3 A `1 i4 C: [' Shttp://www.ncbi.nlm.nih.gov/pubmed/21060009
; f ~# X4 x+ ]/ }# s EArch Neurol. 2010 Nov;67(11):1316-22.
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% m4 q, e6 R) v# V0 _2 L8 rEmerging role of epigenetics in stroke: part 1: DNA methylation and chromatin modifications.
# i- a* f& h9 nQureshi IA, Mehler MF., n8 U, Y% y* g
) m1 ?8 ?1 E& k9 y h6 s+ D+ HRosyln and Leslie Goldstein Laboratory for Stem Cell Biology and Regenerative Medicine, Institute for Brain Disorders and Neural Regeneration, and Rose F. Kennedy Center for Research on Intellectual and Developmental Disabilities, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
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/ P; o4 L; r5 z9 x$ j2 [$ O( k5 h& d0 xAbstract" R( k0 l! k0 y, E, ~
Epigenetic mechanisms refer to the complex and interrelated molecular processes that dynamically modulate gene expression and function within every cell in the body. These regulatory systems represent the long-sought-after molecular interfaces that mediate gene × environment interactions. Changes in the epigenome throughout life are responsible not only for controlling normal development, adult homeostasis, and aging but also for mediating responses to injury. Emerging evidence implicates a spectrum of epigenetic processes in the pathophysiology of stroke. In this review, we describe conventional epigenetic mechanisms (including DNA methylation, histone code modifications, nucleosome remodeling, and higher-order chromatin formation) and highlight the emerging roles each of these processes play in the pathobiology of stroke. We suggest that understanding these mechanisms may be important for discovering more sensitive and specific biomarkers for risk, onset, and progression of stroke. In addition, we highlight epigenetic approaches for stroke therapy, including the inhibition of DNA methyltransferase and histone deacetylase enzyme activities. These therapeutic approaches are still in their infancy, but preliminary results suggest that contemporary agents targeting these pathways can regulate the deployment of stress responses that modulate neural cell viability and promote brain repair and functional reorganization. Indeed, these agents even appear to orchestrate sophisticated cognitive functions, including learning and memory.+ n3 Z* K$ s& f9 p" l9 ^2 D
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