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Segregation of lipid raft markers including CD133 in polarized human hematopoietic stem and progenitor cells. | LitMetric

AI Article Synopsis

  • Hematopoietic stem and progenitor cells can migrate throughout life, but the mechanisms behind their migration are not well understood compared to leukocytes in inflammation.
  • Research showed that human CD34(+) hematopoietic cells develop a polarized shape with distinct front and rear ends when cultivated, similar to migrating leukocytes.
  • Polarization in these cells, which aids in their movement, is triggered by early acting cytokines and involves phosphoinositol-3-kinase activity, indicating common migration processes for both cell types.

Article Abstract

During ontogenesis and the entire adult life hematopoietic stem and progenitor cells have the capability to migrate. In comparison to the process of peripheral leukocyte migration in inflammatory responses, the molecular and cellular mechanisms governing the migration of these cells remain poorly understood. A common feature of migrating cells is that they need to become polarized before they migrate. Here we have investigated the issue of cell polarity of hematopoietic stem/progenitor cells in detail. We found that human CD34(+) hematopoietic cells (1) acquire a polarized cell shape upon cultivation, with the formation of a leading edge at the front pole and a uropod at the rear pole; (2) exhibit an amoeboid movement, which is similar to the one described for migrating peripheral leukocytes; and (3) redistribute several lipid raft markers including cholesterol-binding protein prominin-1 (CD133) in specialized plasma membrane domains. Furthermore, polarization of CD34(+) cells is stimulated by early acting cytokines and requires the activity of phosphoinositol-3-kinase as previously reported for peripheral leukocyte polarization. Together, our data reveal a strong correlation between polarization and migration of peripheral leukocytes and hematopoietic stem/progenitor cells and suggest that they are governed by similar mechanisms.

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Source
http://dx.doi.org/10.1182/blood-2004-02-0511DOI Listing

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