Search

Abstract Lympho-hematopoiesis is regulated by cytokines; however, it remains unclear how cytokines regulate hematopoietic stem cells (HSCs) to induce production of lymphoid progenitors. Here, we show that in mice whose CXC chemokine ligand 12 (CXCL12) is deleted from half HSC niche cells, termed CXC chemokine ligand 12 (CXCL12)-abundant reticular (CAR) cells, HSCs migrate from CXCL12-deficient niches to CXCL12-intact niches. In mice whose CXCL12 is deleted from all Ebf3+/leptin receptor (LepR)+ CAR cells, HSCs are markedly reduced and their ability to generate B cell progenitors is reduced compared with that to generate myeloid progenitors even when transplanted into wild-type mice. Additionally, CXCL12 enables the maintenance of B lineage repopulating ability of HSCs in vitro. These results demonstrate that CAR cell-derived CXCL12 attracts HSCs to CAR cells within bone marrow and plays a critical role in the maintenance of HSCs, especially lymphoid-biased or balanced HSCs. This study suggests an additional mechanism by which cytokines act on HSCs to produce B cells.

Hematopoietic stem cells (HSCs) reside in and are maintained by special microenvironments, termed niches. It is assumed that the HSC niche space remains occupied by endogenous cells and that myelosuppressive conditioning is required to achieve high levels of HSC engraftment. We herein demonstrate that upon the transplantation of very large numbers of purified HSCs into normal mice not exposed to myeloablation, donor HSCs engrafted in niches distant from filled HSC niches without replacing host HSCs and subsequently proliferated and generated hematopoietic progenitors, leading to marked increases in the overallHSCnumbersin bone marrow. Additionally, stem cell factor that is produced by CXC chemokine ligand 12-abundant reticular cells is involved in HSC engraftment. In contrast, host granulocyte/macrophage progenitors (GMPs) were replaced by the progeny of transplanted donor HSCs, and overall GMP numbers remained unchanged. Thus, inconsistent with the classical concept, numerous empty HSC niches are available for engraftment and proliferation in bone marrow. [ABSTRACT FROM AUTHOR]

In this study, the availability of chitosan was systematically investigated for removal of bisphenol A BPA, 2,2bishydroxyphenylpropane through the tyrosinasecatalyzed quinone oxidation and subsequent quinone adsorption on chitosan beads. In particular, the process parameters, such as the hydrogen peroxide H2O2toBPA ratio, pH value, temperature, and tyrosinase dose, were discussed in detail for the enzymatic quinone oxidation. Tyrosinasecatalyzed quinone oxidation of BPA was effectively enhanced by adding H2O2and the optimum conditions for BPA at 0.3 mMwere determined to be pH 7.0 and 40°C in the presence of H2O2at 0.3 mMH2O2BPA 1.0. Removal of BPA from aqueous solutions was accomplished by adsorption of enzymatically generated quinone derivatives on chitosan beads. The use of chitosan in the form of beads was found to be more effective because heterogeneous removal of BPA with chitosan beads was much faster than homogeneous removal of BPA with chitosan solutions, and the removal efficiency was enhanced by increasing the amount of chitosan beads dispersed in the BPA solutions and BPA was completely removed by quinone adsorption in the presence of chitosan beads more than 0.10 cm3cm3. In addition, a variety of bisphenol derivatives were completely or effectively removed by the procedure constructed in this study, although the enzyme dose or the amount of chitosan beads was further increased as necessary for some of the bisphenol derivatives used. © 2010 Wiley Periodicals, Inc. J Appl Polym Sci, 2010 [ABSTRACT FROM AUTHOR]

Whereas most hematopoietic stem cells (HSC) are quiescent in homeostasis, they actively proliferate in response to bone marrow (BM) injury. Signals from the BM microenvironment are thought to promote entry of HSC into the cell cycle. However, it has been cumbersome to assess cycle status of viable HSC and thus explore unique features associated with division. In this study, we show that expression of endothelial cell-selective adhesion molecule (ESAM) can be a powerful indicator of HSC activation. ESAM levels clearly mirrored the shift of HSC between quiescence and activation, and it was prominent in comparison with other HSC-related Ags. ESAMhi HSC were actively dividing, but had surprisingly high long-term reconstituting capacity. Immunohistochemical analyses showed that most ESAMhi HSC were located near vascular endothelium in the BM after 5-fluorouracil treatment. To determine the importance of ESAM in the process of BM recovery, ESAM knockout mice were treated with 5-fluorouracil and their hematopoietic reconstruction was examined. The ESAM deficiency caused severe and prolonged BM suppression, suggesting that ESAM is functionally indispensable for HSC to re-establish homeostatic hematopoiesis. With respect to intracellular regulators, NF-KB and topoisomerase II levels correlated with the ESAM upregulation. Thus, our data demonstrate that the intensity of ESAM expression is useful to trace activated HSC and to understand molecular events involved in stem cell states. [ABSTRACT FROM AUTHOR]