Developmental changes of CD34 expression by murine hematopoietic stem cells

Itô, Tatsuya; Tajima, Fumihito; Ogawa, Makio

doi:10.1016/s0301-472x(00)00535-x

Cited by 104 publications

(80 citation statements)

References 14 publications

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“…Fetal and preadult HSCs are predisposed to stress-independent proliferative expansion, which is, in part, reflected in higher CD34 expression levels compared with adult, quiescent HSCs (Ito et al, 2000;Mikkola and Orkin, 2006;Wilson et al, 2008). Fittingly, we found an increase in activated, CD34 + CD150 + early progenitors in preadult (2 wk old) BM LSK cells from both SIRT1 / and control mice when compared with 5-mo-old adult mice (Fig.…”

Section: Induced Sirt1 Ablation Results In Expansion Of Adult Hspcsmentioning

confidence: 54%

Sirt1 ablation promotes stress-induced loss of epigenetic and genomic hematopoietic stem and progenitor cell maintenance

Singh¹,

Williams²,

Klarmann³

et al. 2013

J Cell Biol

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The (histone) deacetylase Sirt1 is a mediator of genomic and epigenetic maintenance, both of which are critical aspects of stem cell homeostasis and tightly linked to their functional decline in aging and disease. We show that Sirt1 ablation in adult hematopoietic stem and progenitor cells (HSPCs) promotes aberrant HSPC expansion specifically under conditions of hematopoietic stress, which is associated with genomic instability as well as the accumulation of DNA damage and eventually results in a loss of long-term progenitors. We further demonstrate that progenitor cell expansion is mechanistically linked to the selective upregulation of the HSPC maintenance factor and polycomb target gene Hoxa9. We show that Sirt1 binds to the Hoxa9 gene, counteracts acetylation of its histone target H4 lysine 16, and in turn promotes polycomb-specific repressive histone modification. Together, these findings demonstrate a dual role for Sirt1 in HSPC homeostasis, both via epigenetic regulation of a key developmental gene and by promoting genome stability in adult stem cells.

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Section: Induced Sirt1 Ablation Results In Expansion Of Adult Hspcsmentioning

confidence: 54%

Sirt1 ablation promotes stress-induced loss of epigenetic and genomic hematopoietic stem and progenitor cell maintenance

Singh¹,

Williams²,

Klarmann³

et al. 2013

J Cell Biol

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“…[2][3][4] In our laboratory, we observed that the developmental change of CD34 expression from positive to negative state takes place between 7 and 10 weeks of age for most of murine HSCs. 5 We also discovered that CD34 expression by adult stem cells is influenced by the activation state of the HSCs. 2 Regarding stem cell CD38 expression, investigators in four different laboratories including ours reported that HSCs in yolk sac, fetal liver and adult mouse bone marrow express CD38.…”

Section: Introductionmentioning

confidence: 92%

“…5,12 We therefore tested the engraftment capabilities of CD38 − and CD38 + subpopulations of CD34 + bone marrow cells of newborn mice using the FACS regions shown in Figure 1. Because the ratio of the CD34 + CD38 − (R1) cells to CD34 + CD38 + (R2) cells was 20:1, 9.0 × 10 3 CD34 + CD38 − or 4.5 × 10 2 CD34 + CD38 + cells were transplanted into each recipient mouse.…”

Section: Cd38 Expression By Hscs Of Newborn Micementioning

confidence: 99%

“…Because we and other investigators documented that all bone marrow HSCs of 5-week-old and younger mice are CD34 + , 5,12 we set electronic sorting gates as shown in Figure 3. Since the ratio of the CD34 + CD38 − (R3) cells to the CD34 + CD38 + (R4) cells was 5:1, we transplanted 8.0 × 10 4 CD34 + CD38 − cells or 1.6 × 10 4 CD34 + CD38 + cells per mouse.…”

Section: Cd38 Expression By Hscs Of 5-week-old Micementioning

confidence: 99%

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CD38 expression by hematopoietic stem cells of newborn and juvenile mice

2003

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While investigators in a number of laboratories have documented that the hematopoietic stem cells (HSCs) of fetal and adult mice are CD38 + , no information is available about CD38 expression by HSCs of newborn and juvenile mice. We used a murine transplantation model to examine HSC CD38 expression. First, we observed that all HSCs from newborn bone marrow are CD38 − . Next, it was determined that the majority of HSCs in the bone marrow of 5-week-old mice are CD38 − , with a minority being CD38 + . These observations indicated that the CD38 + subpopulation of HSC appears before the age of 5 weeks and expands during adolescence. However, the majority of HSCs of 5-week-old mice became CD38 + following injection of 5-fluorouracil, indicating that activation of juvenile stem cells enhances CD38 expression. These observations may have implications for CD38 expression by HSCs from human umbilical cord blood and bone marrow of young children in steady state and under pathological conditions.

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“…Trabalhos sobre a viabilidade das CT são necessários, já que há dúvidas se os andrógenos afetam a sobrevivência desse tipo de célula (KIM et al, 2005). Além disso, a identificação de marcadores moleculares de superfície dos fenótipos das CT hematopoéticas, como o CD34+, é importante no transplante clínico e na terapia gênica (ITO et al, 2000).…”

Section: IIIunclassified