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[E. Immunology] E-13



               The role of reactive oxygen species (ROS) in hematopoietic


                                          stem cells engraftment




            Minji Choi¹, Mina Boo¹,³, Woo Yong Park²,³, Gahee Song²,³, Ja Yeon Park²,³, Se Jin Jung²,³,

                                  Jinbong Park²,³, Jae-Young Um²,³, Hyun Jeong Kwak¹*

           ¹Department of Natural Science, College of Convergence and Integrated Science, Kyonggi University, Suwon

          16227, Korea, ²Department of sience of Korean Medicine, Graduate school, Kyung Hee University, Seoul 02447,
           Korea, ³Department of pharmacology, Collage of Korean Medicine, Kyung Hee University, Seoul 02447, Korea




        Hematopoietic stem cell transplantation (HSCT) can be curative for hematological and immunological diseases. The

        success of HSCT is dependent on their ability of homing and engraftment to the hematopoietic stem cells (HSCs)
        of recipients. Reactive oxygen species (ROS) is traditional second messengers in many cell type including HSCs,

        however  high  levels  of  ROS  exhausted  hematopoietic  stem  cells  (HSCs).  Therefore,  in  this  study  we  evaluated
        whether maintaining a low levels of ROS in HSCs may augment the engraftment efficiency of HSCs. Transplantation

        of donor BM cells (CD45.1+) into recipients mice (CD45.2+) with a GSH biosynthesis inhibitor, buthionine sulfoximine
        (BSO) displayed a significant increase in HSC engraftment, and this was perturbed in the presence of ROS scavenger,

        N-acetyl-L-cysteine (NAC). In comparison with control mice, BSO-treated recipients displayed a 9.5 fold increase in
        hematopoietic engraftment. Specifically, engraftment efficiency was lower in 25 mg/kg BSO-treated mice than in 5

        mg/kg BSO. Moreover, granulocyte/macrophage progenitors (GMPs) populations was increased in recipient mice,
        suggesting that enhancement of cell differentiation and proliferation of myeloid progenitor cells. Taken together,

        our results suggest a diverse role of ROS that regulates HSC function. Therefore, low ROS has the potential as a
        therapeutic approach in HSCT.
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