Several lines of evidence support the presence of pluripotent stem cells (PSC) in adult bone marrow (BM) and cord blood (CB). To support this, the expression of typical PSC markers Oct-4 and Nanog (embryonic stem cells transcription factors) and SSEA (stage specific embryonic antigen) was reported at the protein and/or mRNA level in BM- and CB-derived stem cells. Accordingly, these embryonic markers were demonstrated in described by our team very small embryonic-like (VSEL) stem cells isolated from the adult bone marrow and cord blood (Leukemia 2006;20:857-869 & Leukemia 2007;21:297-303), multipotent adult progenitor cells (MAPC), mesenchymal stem cells (MSC) and marrow-isolated adult mulitlineage inducible (MIAMI) cells.

In addition to BM and CB, recently several groups reported the presence of Oct-4⁺ cells in epidermis, heart, pancreas, testis, and bronchial epithelium. Since SSEA, Oct-4 and Nanog are the markers characteristic for embryonic stem cells (ESC), epiblast stem cells (EPSC) and primordial germ cells (PGC), the presence of these cells in adult tissues supports the concept that adult tissues contain some population of PSC that is deposited in embryogenesis during early gastrulation. We hypothesize that these cells could be direct descendants of the germ lineage. The germ lineage in order to pass genes on to the next generations creates soma and thus becomes a “mother lineage” for all somatic cell lineages present in the adult body. We also hypothesize that similarly as PGC, PSC deposited in the developing tissues undergo erasure of their somatic imprint. This mechanism of erasure will protect developing organism from the possibility of teratoma formation. However, it also affects some of the aspects of the “true pluripotentiality” of these cells (e.g., their potential to complete blastocyst development).

We postulate that these Oct-4⁺ PSC play a role in steady state conditions in tissue turnover (e.g., as source of long term hematopoiesis repopulating cells). Furthermore, during organ damage (e.g., heart infarct or stroke) these cells could be mobilized from the BM and perhaps other tissue specific niches into peripheral blood where they circulate in order to “home” to damaged organs and participate in their repair (Circulation 2004, 110, 3213-3220, Cir. Research 2004, 95, 1191-1199, Exp. Hematol. 2005, 33, 613-623, Leukemia 2006, 20, 18-28). On other hand they may be also a source of malignancies. Accordingly, if these cells i) do not erase somatic imprint, ii) go astray from the major migratory routes, iii) acquire critical mutations or iv) if mobilized at the wrong time into peripheral blood, and deposited in areas of chronic inflammation, instead of playing a role in regeneration may contribute to the development of malignancies (e.g., teratomas, germinomas, pediatric sarcomas and development of other tumors respectively) (Stem Cells 2005, 23, 879-894, Leukemia 200, 21, 860-867).

• Legal notice:
  

  Copyright (c) Pielaszek Research, all rights reserved.
  The above materials, including auxiliary resources, are subject to Publisher's copyright and the Author(s) intellectual rights. Without limiting Author(s) rights under respective Copyright Transfer Agreement, no part of the above documents may be reproduced without the express written permission of Pielaszek Research, the Publisher. Express permission from the Author(s) is required to use the above materials for academic purposes, such as lectures or scientific presentations.
  In every case, proper references including Author(s) name(s) and URL of this webpage: https://science24.com/paper/11139 must be provided.

1. The sensitivity of immortalized hybrid endothelial-cancer cells EA.hy926 to UVC radiation in comparison with human promyelocytic leukaemia HL60 cells
2. Arachidonic acid contained in triacylglycerol is a potential factor determining phagocytic function of human monocytes/macrophages
3. Interactions between aluminofluoride complexes (AlF_x) and proline using the methods of molecular modelling.