ESPE2015 Poster Category 2 GH & IGF (40 abstracts)
Analysis of CD133+CD45+ Hematopoietic Progenitor/Stem Cells and CD133+/CD45- Very Small Embryonic-Like Stem Cells in Children with GH Deficiency Subjected to GH Therapy
A Bossowski a , P Singh b , K Grubczak b , U Radzikowska b , B Sawicka a , P Miklasz b , M Dabrowska c , A Bossowska d & M Moniuszko b
aDepartment of Pediatrics Endocrinology, Diabetology with the Cardiology Division, Medical University in Bialystok, Bialystok, Poland; bDepartment of Regenerative Medicine and Immune Regulation, Medical University, Bialystok, Poland; cDepartment of Hematology Diagnostic, Medical University in Bialystok, Bialystok, Poland; dDivision of Cardiology, Internal Affairs Ministry Hospital in Bialystok, Bialystok, Poland
Background: GH deficiency (GHD) is an endocrine condition, caused by problems arising in the pituitary gland that does not produce sufficient quantities of GH. GHD is treated by replacing GH with one daily injections. Recent studies suggested that GH could be involved in regulation of certain stem cell subset potential and function. However, the exact effects of GH therapy on biology of stem cells in paediatric patients were not studied in detail.
Methods: Here we aimed to evaluate the levels of very small embryonic-like cells (VSELs) delineated by Lin-CD133+CD45- phenotype and hematopoietic stem/progenitor cells characterized by Lin-CD133+CD45+ phenotype in relation to treatment with GH. Study groups consisted of children with GH deficiency that were diagnosed with GHD but did not start GH therapy yet; children diagnosed with GHD and treated with GH and healthy controls (HC). Peripheral blood samples were subjected to extracellular staining using fluorochrome-conjugated monoclonal antibodies: anti-CD235 FITC, anti-CD45 PE, anti-CD133 APC, and Lin 1 FITC mixture. Following incubation immunostained blood samples were incubated for with BD FACS Lysing Solution and washed twice to get rid of erythrocytes.
Results: We demonstrated that children with GHD who were treated with GH presented with higher VSEL, and to a lesser extent, HSC levels than untreated GHD patients. Notably, VSEL and HSC levels were significantly higher in GHD patients treated with GH than in HC.
Conclusion: Altogether, we propose that GH therapy in GHD paediatric patients can be associated with expansion of peripheral blood stem and progenitor cells. Further studies assessing the longevity of such phenomenon are still warranted.
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