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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。9 T4 o4 |, K' w3 H
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.
4 N9 ?& H; ?. c: R" ?# 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。
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/ F8 j' F* t1 n- h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。: n5 h0 b0 k6 ~0 U3 {3 V
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Systemic signals regulate ageing and rejuvenation of blood stem cell niches5 ]6 D* F' _. _4 R M# C% G* p
Shane R. Mayack, Jennifer L. Shadrach, Francis S. Kim & Amy J. Wagers4 A$ e$ d2 v5 [, R b4 b, j/ ~
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.
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* w* |. ^2 n$ B& \7 eAgeing 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 supportive3 t5 R; q& P+ N1 Y2 H
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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