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本帖最后由 nanocellmatrix 于 2010-4-24 20:17 编辑
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2 E0 q. i' [ I6 x" B, EHarvard 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。
- M; V0 V8 X* s( F' \ 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.
2 D$ V. d1 Y: @/ f% M 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。7 O$ X8 v' G4 H9 X3 ?3 K
9 A) c: a4 x$ J: M: i2 t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。
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( k& C8 L& V1 U) l( X* ^Systemic signals regulate ageing and rejuvenation of blood stem cell niches, T9 u" N6 b: U) |1 }
Shane R. Mayack, Jennifer L. Shadrach, Francis S. Kim & Amy J. Wagers
, Z Y# F- T$ H, {0 g; C7 wDepartment 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.) T% {3 E; R& P6 T
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* z5 E* H+ C! {" ?2 oAgeing 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% H8 p/ P, T+ `; h0 ]! u
microenvironment, 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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