The magic of CD 34 positive cells

The magic of CD 34 positive cells

The discovery of the CD34 cell-surface antigen involved the use of monoclonal antibodies specific for progenitors of hematopoietic cells. This led to the use of purifying hematopoietic cells in the blood and bone marrow easily to treat a host of diseases. CD 34 is described as spanning the plasma membrane making it a transmembrane protein-its ligand is l-Selectin (CD62L) while another protein called CrkL also binds to it.

Apart from blood cells, CD 34 has also been shown to be present on multipotent mesenchymal stromal cells (MSCs), embryonic fibroblasts, vascular endothelial progenitors, epithelial progenitors and interstitial dendritic cells, according to 2014-published research in Stem cells (Dayton, Ohio).

At a clinical level, the expression of CD 34 serves as a check of the rapid engraftment in bone marrow transplants. It also allows the enrichment of immature hematopoietic cells by cell sorting. The presence of CD 34 also serves as an identification of hematopoietic stem cells /progenitors. Such CD34+ hematopoietic stem cells show the high capacity of cell division. They can differentiate into cells of the hematopoietic lineage as well as other lineages such as cardiomyocytes, hepatocytes and epithelial cells of the respiratory system (Sidney and team, 2014).

The functions of this protein remain to be assessed in detail. However, from available research, the functions range from adhesion of cells and regulation of cell division and differentiation in hematopoietic cells. The trafficking of HSC to niches within the bone marrow also involves the role of CD 34. The protein is also involved in haematopoiesis and facilitates the adhesion of lymphocytes to L-selectin. The protein also prevents integrin activation to cause steric hindrance of adhesion mediated by integrins in hematopoietic stem cells.

Early research showed that the hematopoietic system of primates that received irradiation was reconstituted by CD34+ cells. This engraftment was also seen in human cancers such as breast cancer and neuroblastoma. 2011-published research in the Texas Heart Institute journal reported that humans receiving myeloablative therapy were administered CD34+ for hematopoietic reconstitution.

The promise of CD 34+ cells in cell therapy has also been shown by clinical studies. For example, early research in The American Heart Journal in 2006 reported that functional improvements such as the ventricular volume were seen when patients undergoing coronary artery bypass grafting were administered autologous bone marrow mononuclear cell transplantation. The therapeutic effect seen was attributed to the presence of CD34+ cells.

A trial (unique identifier NCT00081913) explored whether the symptoms seen in intractable angina patients were improved with CD34+ cells. The direct cardiac injections of autologous CD34+cells showed an improvement in the Canadian Cardiovascular Society angina classification scale, frequency of angina and overall quality of life against controls. The absence of any adverse or new events such as heart failure was not reported suggesting the safety of the use of these cells in therapy.

The treatment of several diseases has shown promise with the use of CD 34+ cells ranging from diabetes mellitus to cancer to autoimmune disorders and cardiovascular disease (CVD) (Mackie and Losordo, 2011). Thus, these cells have a wide range of applications to treat diseases and improve the quality of life.

References:

Mackie, A. R., & Losordo, D. W. (2011). CD34-positive stem cells: in the treatment of heart and vascular disease in human beings. Texas Heart Institute Journal38(5), 474–485.

Sidney, L. E., Branch, M. J., Dunphy, S. E., Dua, H. S., & Hopkinson, A. (2014). Concise review: evidence for CD34 as a common marker for diverse progenitors. Stem cells (Dayton, Ohio)32(6), 1380–1389.

Mocini D, Staibano M, Mele Let al. Autologous bone marrow mononuclear cell transplantation in patients undergoing coronary artery bypass grafting. The American Heart Journal. 2006 Jan; 151(1):192-7.

 

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