TNFα induces Caspase-3 activity in hematopoietic progenitor cells CD34+, CD33+, and CD41+of myelodysplastic syndromes

Background Cytopenia is the primary feature of Myelodysplastic Syndrome, even in the presence of hypercellular bone marrow. TNF alpha is recognized as both a proinflammatory, and proapoptotic cytokine with a well established role in promoting apoptosis in MDS. Therefore, TNF alpha has the potential to be a valuable biomarker for predicting the progression of cytopenia in MDS. This study aims to establish the role of TNF alpha exposure in triggering apoptosis through caspase-3 activity in CD34+, CD33+, and CD41 + cells in MDS. Methods This study is an in vitro comparative experimental research. Bone marrow mononuclear cells were isolated as the source of hematopoietic progenitor cells. Subsequently, CD34+, CD33+, and CD41 + cells were exposed to rhTNF alpha, and the caspase-3 activity was measured using flowcytometry. Results In MDS CD33 + and CD41 + caspase-3 activity of rhTNF alpha exposed cells was significantly higher than without exposed cells. The opposite result was found in CD34 + cells, where the caspase-3 activity without rhTNF alpha exposed cells was significantly higher than rhTNF alpha exposed cells. Conclusion rhTNF alpha exposure led to an elevation in caspase-3 activity in MDS progenitor cells, especially in those that had differentiated into myeloid cell CD33 + and megakaryocyte cell CD41+, as opposed to the early progenitor cells CD34+.