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本帖最后由 nanocellmatrix 于 2010-4-24 20:17 编辑
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Harvard 的科学家证实将衰老的造血干细胞培养于年轻的Niche中,衰老的干细胞命运可以逆转。. q$ [& E% S2 p: A
对于这个问题的解答:不外乎stem cell intrinsic alterations 或 age-related changes in the stem cell supportive microenvironment/ niche.0 p& C" I# s! W$ m+ D
研究发现,这种现象与niche细胞应答有关,同时与局部微环境中IGF的调节有关。& j3 L: s; r+ i+ b, D; R# N, @
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希望大家可以关于干细胞命运的逆转(ips,衰老,转分化等)探讨。: U+ j! F; D0 \5 c' x
X( q0 k2 m0 i2 I6 }" FSystemic signals regulate ageing and rejuvenation of blood stem cell niches
. p: [/ H0 Z. S& sShane R. Mayack, Jennifer L. Shadrach, Francis S. Kim & Amy J. Wagers! i; W' R8 G7 Q) [. Z
Department of Stem Cell and Regenerative Biology, Harvard University, Howard Hughes Medical Institute, Harvard Stem Cell Institute, Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02115, USA.) a8 Q( ~4 I( {' a
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Ageing in multicellular organisms typically involves a progressive decline in cell replacement and repair processes, resulting in several physiological deficiencies, including inefficient muscle repair, reduced bone mass, and dysregulation of blood formation (haematopoiesis). Although defects in tissue-resident stem cells clearly contribute to these phenotypes, it is unclear to what extent they reflect stem cell intrinsic alterations or age-related changes in the stem cell supportive
% K: h2 E& G( [/ y/ w1 B) tmicroenvironment, or niche. Here, using complementary in vivo and in vitro heterochronic models, we show that age-associated changes in stem cell supportive niche cells deregulate normal haematopoiesis by causing haematopoietic stem cell dysfunction. Furthermore, we find that age-dependent defects in niche cells are systemically regulated and can be reversed by exposure to a young circulation or by neutralization of the conserved longevity regulator, insulin-like growth factor-1, in the marrow microenvironment. Together, these results show a new and critical role for local and systemic factors in signalling age-related haematopoietic decline, and highlight a new model in which blood-borne factors in aged animals act through local niche cells to induce age-dependent disruption of stem cell function. |
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