Heterochronic parabiosis for the study of the effects of aging on stem cells and their niches

被引:211
作者
Conboy, Irina M. [1 ,2 ]
Rando, Thomas A. [3 ,4 ,5 ,6 ]
机构
[1] Univ Calif Berkeley, Dept Bioengn, Berkeley, CA 94720 USA
[2] Univ Calif Berkeley, Inst QB3, Berkeley, CA 94720 USA
[3] Stanford Univ, Sch Med, Paul F Glenn Labs Biol Aging, Stanford, CA 94305 USA
[4] Stanford Univ, Sch Med, Dept Neurol & Neurol Sci, Stanford, CA 94305 USA
[5] Vet Affairs Palo Alto Hlth Care Syst, Neurol Serv, Palo Alto, CA USA
[6] Vet Affairs Palo Alto Hlth Care Syst, Rehabil Res & Dev Ctr Excellence, Palo Alto, CA USA
关键词
aging; parabiosis; stem cells; niche; muscle; AGE-RELATED-CHANGES; SISTER CHROMATIDS; MUSCLE; ADULT; OLD; NEUROGENESIS; SEGREGATION; NOTCH; DNA; YOUNG;
D O I
10.4161/cc.20437
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Aging is unmistakable and undeniable in mammals. Interestingly, mice develop cataracts, muscle atrophy, osteoporosis, obesity, diabetes and cognitive deficits after just 2-3 postnatal years, while it takes seven or more decades for the same age-specific phenotypes to develop in humans. Thus, chronological age corresponds differently with biological age in metazoan species and although many theories exist, we do not understand what controls the rate of mammalian aging. One interesting idea is that species-specific rate of aging represents a ratio of tissue attrition to tissue regeneration. Furthermore, current findings suggest that the age-imposed biochemical changes in the niches of tissue stem cells inhibit performance of this regenerative pool, which leads to the decline of tissue maintenance and repair. If true, slowing down stem cell and niche aging, thereby promoting tissue regeneration, could slow down the process of tissue and organismal aging. In this regard, recent studies of heterochronic parabiosis provide important clues as to the mechanisms of stem cell aging and suggest novel strategies for enhancing tissue repair in the old. Here we review current literature on the relationship between the vigor of tissue stem cells and the process of aging, with an emphasis on the rejuvenation of old tissues by the extrinsic modifications of stem cell niches.
引用
收藏
页码:2260 / 2267
页数:8
相关论文
共 62 条
[1]
TNF Inhibits Notch-1 in Skeletal Muscle Cells by Ezh2 and DNA Methylation Mediated Repression: Implications in Duchenne Muscular Dystrophy [J].
Acharyya, Swarnali ;
Sharma, Sudarshana M. ;
Cheng, Alfred S. ;
Ladner, Katherine J. ;
He, Wei ;
Kline, William ;
Wang, Huating ;
Ostrowski, Michael C. ;
Huang, Tim H. ;
Guttridge, Denis C. .
PLOS ONE, 2010, 5 (08)
[2]
Bert P., 1864, J Anat. Physiol, V1, P69
[3]
A temporal switch from Notch to Wnt signaling in muscle stem cells is necessary for normal adult myogenesis [J].
Brack, Andrew S. ;
Conboy, Irina M. ;
Conboy, Michael J. ;
Shen, Jeanne ;
Rando, Thomas A. .
CELL STEM CELL, 2008, 2 (01) :50-59
[4]
Increased Wnt signaling during aging alters muscle stem cell fate and increases fibrosis [J].
Brack, Andrew S. ;
Conboy, Michael J. ;
Roy, Sudeep ;
Lee, Mark ;
Kuo, Calvin J. ;
Keller, Charles ;
Rando, Thomas A. .
SCIENCE, 2007, 317 (5839) :807-810
[5]
BCL9 is an essential component of canonical Wnt signaling that mediates the differentiation of myogenic progenitors during muscle regeneration [J].
Brack, Andrew S. ;
Murphy-Seiler, Fabienne ;
Hanifi, Jasmine ;
Deka, Juergen ;
Eyckerman, Sven ;
Keller, Charles ;
Aguet, Michel ;
Rando, Thomas A. .
DEVELOPMENTAL BIOLOGY, 2009, 335 (01) :93-105
[6]
MUTATION SELECTION AND NATURAL-HISTORY OF CANCER [J].
CAIRNS, J .
NATURE, 1975, 255 (5505) :197-200
[7]
Restoring production of hippocampal neurons in old age [J].
Cameron, HA ;
McKay, RDG .
NATURE NEUROSCIENCE, 1999, 2 (10) :894-897
[8]
CARLSON BM, 1989, AM J PHYSIOL, V256, pC1262
[9]
Imbalance between pSmad3 and Notch induces CDK inhibitors in old muscle stem cells [J].
Carlson, Morgan E. ;
Hsu, Michael ;
Conboy, Irina M. .
NATURE, 2008, 454 (7203) :528-U9
[10]
Regulating the Notch pathway in embryonic, adult and old stem cells [J].
Carlson, Morgan E. ;
Conboy, Irina M. .
CURRENT OPINION IN PHARMACOLOGY, 2007, 7 (03) :303-309