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Title: Release of haemopoietic progenitor cells in peripheral blood after acute myocardial infarction
Author: Suresh, Venkatesan
ISNI:       0000 0001 3491 3033
Awarding Body: University of Manchester
Current Institution: University of Manchester
Date of Award: 2008
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We aimed to establish whether and over what time course haemopoietic progenitor cells are released in the peripheral circulation after myocardial infarction (MI) in humans. We investigated the expression of CD34+ and novel stem cell marker CD133+ on peripheral blood stem cell and also the time course of their release after ischaemic insult. We also investigated the stem cell expression of various endothelial markers like CD31+ and CD144+. We recruited 5 patients with acute ST segment elevation MI, 5 patients with non-cardiac chest pain and 5 healthy controls. 20ml of peripheral blood was obtained after informed consent on days 1-7, 15 and 30 on patients with MI and non-cardiac chest pain and days 1, 4 and 7 on healthy controls. There was no significant increase in the haemopoietic progenitor cells in the MI group when compared to the control. Furthermore, these progenitor cells did not show an increased expression of endothelial markers CD31+ and CD144+. Vascular endothelial growth factor (VEGF), granulocyte colony stimulating factor (G-CSF), Interleukin-6 (IL-6) Stromal derived factor (SDF-1a) were significantly elevated in the MI group when compared to healthy controls. The VEGF peaked at day 4 after MI. Other chemo-attractants like monocytes chemo-attractant protein (MCP-1), Interleukin-8 (IL-8) were not elevated. Preliminary results in a small number of patients reveals that haemopoietic progenitor cells are not mobilised in peripheral circulation after myocardial ischaemia. Furthermore these haemopoietic progenitor cells also failed to show increased expression of endothelial markers. These data highlight that haemopoietic progenitor cell mobilisation does not occur in all patients with myocardial ischaemia and that de novo release of progenitor cells from the bone marrow is unlikely to be an important mechanism for myocardial repair.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (M.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available