干细胞衰老以及逆转

nanocellmatrix

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" W5 L7 B7 w) y5 K$ a+ wHarvard 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。& S2 t# q3 U- ~3 r: J4 P
   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.' I- e5 s) `+ U  T! ?
     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。5 ^6 J, x, i* S, e" T# f; F, s

- l1 J8 @# d0 z% w9 e  f% \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。; i, ^! c+ T- r) W: @2 [+ l
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Systemic signals regulate ageing and rejuvenation of blood stem cell niches" ]/ }  x6 n* ?0 |5 X0 g
Shane R. Mayack, Jennifer L. Shadrach, Francis S. Kim & Amy J. Wagers* I  \: b& @6 c8 W8 o* w
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.# a$ o& q, T' D" b& `5 a7 P

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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 supportive5 S; n/ m! Z- t" }$ T- }
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.