Transit-Amplifying Cell Frequency and Cell Cycle Kinetics Are Altered in Aged Epidermis

被引:32
作者
Charruyer, Alexandra
Barland, Chantal O.
Yue, Lili
Wessendorf, Heike B.
Lu, Ying [2 ]
Lawrence, H. Jeffrey [3 ]
Mancianti, Maria L. [4 ]
Ghadially, Ruby [1 ,5 ]
机构
[1] Univ Calif San Francisco, Vet Affairs Med Ctr, Dept Dermatol, San Francisco, CA 94121 USA
[2] Univ Calif San Francisco, Dept Radiol, San Francisco, CA 94121 USA
[3] Vet Affairs Med Ctr, Dept Med, San Francisco, CA 94121 USA
[4] Alta Bates Med Ctr, Dept Pathol, Berkeley, CA USA
[5] VA Med Ctr San Francisco, Dept Dermatol, San Francisco, CA USA
关键词
HEMATOPOIETIC STEM-CELLS; IN-VIVO; SURFACE PHENOTYPE; MOUSE; SKIN; PROLIFERATION; KERATINOCYTES; POPULATION; VITRO; DIFFERENTIATION;
D O I
10.1038/jid.2009.127
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100227 [皮肤病学];
摘要
Aged epidermis is less proliferative than young, as exemplified by slower wound healing. However, it is not known whether quantitative and/or qualitative alterations in the stem and/or transit-amplifying ( TA) compartments are responsible for the decreased proliferation. Earlier studies found a normal or decreased frequency of putative epidermal stem cells (EpiSCs) with aging. We show, using long-term repopulation in vivo and colony formation in vitro, that, although no significant difference was detected in EpiSC frequency with aging, TA cell frequency is increased. Moreover, aged TA cells persist longer, whereas their younger counterparts have already differentiated. Underlying the alteration in TA cell kinetics in the aged is an increase in the proportion of cycling keratinocytes, as well as an increase in cell cycle duration. In summary, although no significant difference in EpiSC frequency was found, TA cell frequency was increased ( as measured by in vivo repopulation, growth fraction, and colony formation). Furthermore, the proliferative capacity ( cellular output) of individual aged EpiSCs and TA cells was decreased compared to that of young cells. Although longer cell cycle duration contributes to the decreased proliferative output from aged progenitors, the greater number of TA cells may be a compensatory mechanism tending to offset this deficit.
引用
收藏
页码:2574 / 2583
页数:10
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