- 积分
- 13286
- 威望
- 13286
- 包包
- 34831
|
本帖最后由 sunsong7 于 2011-5-16 23:34 编辑
% n. F3 ^1 |6 u/ F) N" V: ^6 H张也行 发表于 2011-5-16 22:20 3 n* c( |, o; P; o% W
回复 sunsong7 的帖子/ e' p" w- \) m% `6 y; \
% \; \( i9 @! J. ]: C9 i"如果终末细胞不具备进行“复制”或“增殖”的潜能还不能被称为“细胞”" 5 d! ^% E# O! K4 c/ }/ R$ h+ M
: N$ j) u0 S" j% @" _7 D. q1 i$ d
关于不能复制的细胞是否还算“细胞”?这个问题请参看前面贴子关于细胞的定义(http://www.stemcell8.cn/forum-re ... 657-pid-360678.html)
1 N! [" v5 s5 k5 C另外,一些研究表明除了“重编程”技术外,病毒感染、细胞微环境改变等因素可以再激活终末分化细胞进入细胞周期,说明终末分化细胞仍具有可塑性。4 _; |- a# Q6 M, @
% E3 p. K3 a! j0 ~! @$ d, ~6 L. Q b- X7 x8 d0 T
【扩展阅读】3 V/ U2 X U, C0 N
通常理解,终末分化细胞(terminally differentiated cells) 又称不育细胞或不分裂细胞,指一旦生成后,终生不再分裂的高度分化的成熟细胞。简单地说就是最后定型的细胞,干细胞进入终末分化后,形成执行特定功能的成熟细胞,不再分裂,譬如运输氧气的红细胞、成熟表皮细胞、神经元、成熟的浆细胞等等。. x- ~7 m5 D5 [' V) s; ^% _
0 q3 \( v6 `/ Q: B! w8 u% k! d ?
类似的概念还有永久性细胞(permanent cells)是指不具有再生能力的细胞,此类细胞出生后即脱离细胞周期,永久停止有丝分裂。 属于此类的有神经细胞(包括中枢的神经元和外周的节细胞),另外心肌细胞和骨骼肌细胞再生能力也极弱,没有再生修复的实际意义,一旦损伤破坏则永久性缺失,代之以瘢痕性修复。# A. |1 I E/ q* ]
- x+ A2 B% j* k$ y! L
下面的资料表明这些观点正在被颠覆:
$ U* p2 Y) w) U+ Q' G; p/ D- D6 L$ U# n3 ^. i. M& P
Terminally differentiated skeletal myotubes are not confined to G0 but can enter G1 upon growth factor stimulation (终末分化细胞并不仅锁定于G0期,细胞因子可以刺激其进入G1期)) p G1 u- R( c
M Tiainen, D Pajalunga, F Ferrantelli, S Soddu, G Salvatori, A Sacchi and M Crescenzi 3 Q* v* F% o1 s; P% m4 C) E& J
Molecular Oncogenesis Laboratory Regina Elena Cancer Center, Rome, Italy. * w) ]: |. m/ P. c, t& {( ^
Cell Growth & Differentiation, Vol 7, Issue 8 1039-1050, Copyright © 1996 by American Association of Cancer Research + D# } s: h, m. K' N( I+ N
Terminally differentiated cells are specialized cells unable to proliferate that constitute most of the mammalian body. Despite their abundance, little information exists on the characteristics of cell cycle control in these cells and the molecular mechanisms that prevent their proliferation. They are generally believed to be irreversibly restricted to the G0 state. In this report, we define some features of a paradigmatic terminally differentiated system, the skeletal muscle, by studying its responses to various mitogenic stimuli. We show that forced expression of a number of cell cycle-regulatory genes, including erbB-2, v-ras, v-myc, B-myb, ld-1, and E2F-1, alone or in combinations, cannot induce terminally differentiated skeletal muscle cells (myotubes) to synthesize DNA. However, serum-stimulated myotubes display a typical immediate-early response, including the up-regulation of c-fos, c-jun, c-myc, and ld-1. They also elevate the expression of cyclin D1 after 4 hours of serum treatment. All these events take place in myotubes in a way that is indistinguishable from that of quiescent, undifferentiated myoblasts reactivated by serum. Moreover, pretreatment with serum shortens the time required by E1A to induce DNA synthesis, confirming that myotubes can partially traverse G1. Serum growth factors do not activate late-G1 genes in myotubes, suggesting that the block that prevents terminally differentiated cells from proliferating acts in mid-G1. Our results show that terminally differentiated cells are not confined to G0 but can partially reenter G1 in response to growth factors; they contribute to a much-needed definition of terminal differentiation. The important differences in the control of the cell cycle between terminally differentiated and senescent cells are discussed.
" i+ S3 ?6 B5 a' y+ R* i2 k: J. A1 ]( U n4 A' Q& X# A; t
( [7 N3 V" y- K( C- q d# U5 ?( {6 _! |
Reactivation of the Cell Cycle in Terminally Differentiated Cells (终末分化细胞的细胞周期再激活)% b* l M- a7 z; H
Molecular Biology Intelligence Unit 17, by Marco Crescenzi, Publisher: Springer 2003
- b& \) y* c- @. y
" p( {$ `) w7 x; a. aTerminal differentiation is defined as the state in which a cell has acquired specialized properties and has ceased proliferating permanently. This book comprehensively describes whether the terminally differentiated state actually exists, the molecular mechanisms that control the post-mitotic state, and whether terminally differentiated cells can be induced to proliferate in a stable, controllable and reversible fashion.6 W+ q$ D8 i, X S; e* B
! t4 P5 c' Z/ L' }
This volume deals with the most advanced areas of reactivation of the cell cycle in terminally differentiated cells. Terminally differentiated cells have long been regarded as irreversibly unable to proliferate. However, this view is being overturned, with great implications for both biological knowledge and potential therapeutic applications.
* b; M0 ]1 p4 Q u' c* U0 m
' l8 ?0 D- T5 GTable of Contents( o8 d1 x; u- j, i& z
Reactivation of Terminally Differentiated Cells: Introduction Marco Crescenzi5 A5 b$ [7 l! U" a1 K- Q! ^$ S4 ^
Cell cycle reactivation in skeletal musce cells Marco Crescenzi ( z' p: ^6 \: v7 |1 e H
Myocyte Proliferation in the Failing Heart Piero Anversa M5 O5 K! b! Q
Reversal of terminally differentiated state in skeletal myocytes by SV40 large T antigen Takeshi Endo
+ e2 r; \4 X( @; x6 c0 c+ _' bRegulation of proliferation and apoptosis in the cardiac myocyte Loren J. Field
( a9 i2 A* p" w3 L" dThe "Post-mitotic" Phenotype in Cardiac Muscle Cells Michael D. Schneider8 u. _5 F- ?7 I2 b
Cellular de-differentiation during regeneration: the amphibian muscle system Elly M. Tanaka
, d2 ? o- o! b4 e% C( X【在线阅读】http://www.ccebook.net/preview/0 ... ifferentiated-cells7 |# @( {, Y% B) G s
7 m6 `) @8 w5 Z# s- ~# S7 d
Mitotic cycle reactivation in terminally differentiated cells by adenovirus infection. (腺病毒感染可再激活终末分化细胞进行有丝分裂)4 j: T/ V" s5 ? @' A h! k3 p
Journal of cellular physiology, Vol. 162, No. 1. (January 1995), pp. 26-35. doi:10.1002/jcp.1041620105 Key: citeulike:3503872
+ y: f' r u+ h9 ADifferent cell types (e.g., neurons, skeletal and heart myocytes, adipocytes, keratinocytes) undergo terminal differentiation, in which acquisition of specialized functions entails definitive withdrawal from the cell cycle. Such cells are distinct from quiescent (reversibly growth-arrested) cells, such as contact-inhibited fibroblasts. Terminally differentiated cells can not be induced to proliferate by means of growth factor stimulation or transduction of cellular oncogenes. An important first step toward defining the molecular basis for such unresponsiveness is to find a practical means to overcome the proliferative block. Furthermore, determining whether terminally differentiated, postmitotic cells still retain a potential competence for proliferation that can be reactivated would have important theoretical and practical implications. To address these questions, we exploited the properties of adenoviruses. These viruses can infect postmitotic cells and express E1A, a powerful activator of proliferation in reversibly growth-arrested cells. We infected terminally differentiated skeletal muscle cells and adipocytes with human adenovirus type 5 or 12, obtaining full reentry into the cell cycle, including DNA synthesis, mitosis, cytokinesis, and extended proliferation. Similar results were obtained with established cell lines and primary cells belonging to several species, from quail to humans. Genetic analysis indicated that the smaller splice product of E1A, E1A 12S, is sufficient to induce cell cycle reactivation in otherwise permanently nonmitotic cells. These results demonstrate that terminally differentiated cells retain proliferative potential and establish adenovirus as a convenient and powerful means to force such cells to reenter the cell cycle. (http://www.citeulike.org/user/giovenko/article/3503872)0 B4 E3 p) c; p8 e6 u$ W( Q
|
附件: 你需要登录才可以下载或查看附件。没有帐号?注册
-
总评分: 威望 + 20
包包 + 30
查看全部评分
|