Leukemia cell microvesicles promote survival in umbilical cord blood hematopoietic stem cells

Farnaz Razmkhah1, Masoud Soleimani1, Davood Mehrabani2

  • 1Department of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran.

EXCLI Journal
|February 11, 2016
PubMed

Insights

Leukemia cell microvesicles promote survival of umbilical cord blood hematopoietic stem cells. These microvesicles demonstrated an anti-apoptotic effect, increasing cell count and viability while decreasing P53 gene expression.

Area of Science:

  • Cell Biology
  • Hematology
  • Cancer Research

Background:

  • Microvesicles mediate intercellular communication by transferring proteins and RNA.
  • Microvesicle cargo can influence target cell fate, including apoptosis or survival.
  • Leukemic microvesicles' impact on hematopoietic stem cells requires further investigation.

Purpose of the Study:

  • To investigate the effect of microvesicles derived from leukemic cells on umbilical cord blood hematopoietic stem cells (HSCs).
  • To determine if leukemic microvesicles induce apoptosis or promote survival in HSCs.
  • To analyze changes in cell count, viability, stem cell markers, and P53 gene expression.

Main Methods:

  • Isolation of microvesicles from healthy bone marrow and Jurkat leukemic cells via ultra-centrifugation.
  • Co-culture of umbilical cord blood HSCs with isolated microvesicles.
  • Assessment of cell count, viability, CD34 expression (hematopoietic stem cell marker), and P53 gene expression via qPCR after 7 days.

Main Results:

  • Leukemic microvesicles significantly increased HSCs cell number and viability compared to normal and control groups.
  • P53 gene expression was lower in HSCs treated with leukemic microvesicles.
  • Expression of CD34 marker remained unchanged, and no lineage differentiation was observed.

Conclusions:

  • Leukemic cell-derived microvesicles exert an anti-apoptotic effect on umbilical cord blood HSCs.
  • These findings suggest a potential role for microvesicles in modulating HSC behavior in the context of leukemia.
  • Further research is warranted to elucidate the specific molecular mechanisms involved.

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