כינוס שנתי ה-45 | 2011
פוסטרים להצגה בכינוס
פוסטר זה זכה בפרס שלישי
HIGH DEFINITION FLOW CYTOMETRY PROVIDES CLEAR RESOLUTION OF HSPC AND MK-P POPULATIONS AND THEIR SUBSETS IN NORMAL AND DISEASE STATES
Sigi Kay, Bar-On Shoshi, Ben-Zion Katz, Elizabeth Naparstek and Varda Deutsch,
Department of Haematology and Bone Marrow Transplant, Tel Aviv Medical Centre
and Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel, 6 Weizman St., Tel-Aviv 64239
Thrombopoiesis, which is regulated by physiological demand, requires several steps beginning with hematopoietic stem cell (HSPC) commitment to Mk progenitors (Mk-p), and their expansion followed by terminal Mk maturation and platelet production. While each step in this complex pathway is crucial for platelet production, the Mk-p pool provides the platform for platelet development. Studying Mk-p populations under normal and stress conditions as well as in disease states may provide us with new insights into the molecular and cellular mechanisms that regulate normal and aberrant thrombopoiesis. Using stem cell and Mk specific markers, we studied the flow cytometry profiles of Mk-p and HSPC in normal bone marrow, in mobilized peripheral blood, and cord blood as well as in immune thrombocytopenia purpura (ITP) and in the malignant states, chronic myeloid leukemia (CML) and essential thrombocythemia (ET). Application of multiple gates and high definition flow cytometry (1) enabled clear resolution of different HSPC and Mk-p populations and their early subsets. We demonstrate for the first time that the relative proportion of Mk-p (CD45 low/neg/ SSC low/CD41high) and early Mk-p which still maintain CD34 (CD45 low/neg/ SSC low/CD41high/CD34+), and CD34+ HSPC that have acquired high levels of CD41( CD34 +/SSClow/ CD41high) are not the same under different physiological conditions. Discovering that the flow characteristics of these Mk-p subsets vary in normal and disease states may contribute to our understanding of normal thrombopoiesis, as well as states of refractive thrombocytopenias and excessive thrombopoiesis.
1. Deutsch V, et al., BJH 2010, 149 (1):137-49.

