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This publication is protected and can be accessed only from certain IPs.

Title: Circulation of early hematopoetic, muscle, cardiac, and endothelial tissue-commited stem cell during myocardial infarction

Abstract:

It is assumed that small number of tissue-specific progenitor cells circulate in peripheral blood and the intensified mobilization of the cells from tissue niches, mainly from bone marrow, occurs during acute myocardial infarction. An increase in the number of circulating CD34+, CD117+, c-met+ and CXCR4+ cells in peripheral blood during early period of acute myocardial infarction has been indicated from results of the tests. Simultaneously, a growth in expression of mRNA for cardiac, muscular and endothelial markers among circulating mononuclear cells has been observed. Intensified mobilization of hematopoetic progenitors has been stated in clonogenic in vitro tests. The results of the tests confirmed the hypothesis assuming that the stress involved with myocardial infarction mobilizes tissue-derived stem cells–from tissue niches to peripheral blood. Mobilization of the cells is accompanied by some changes in cytokine concentration in peripheral blood (an increase in VEGF, IL-6, G-CSF and HGF, and a decrease in serum level of SDF-1). The results obtained in the dissertation suggest not only the possibility of circulation of heterogenic population of stem cells in blood but also confirmed the mobilization induced by organ damage in the course of myocardial infarction.

Place of publishing:

Kraków

Level of degree:

2 - studia doktoranckie

Degree discipline:

choroby układu krążenia ; fizjologia ; transplantologia

Degree grantor:

Wydział Lekarski

Promoter:

Ratajczak, Mariusz

Date issued:

2007

Identifier:

oai:dl.cm-uj.krakow.pl:950

Call number:

ZB-106436

Language:

pol

Access rights:

tylko w bibliotece

Object collections:

Last modified:

Feb 4, 2023

In our library since:

Nov 21, 2012

Number of object content hits:

10

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0

All available object's versions:

http://dl.cm-uj.krakow.pl:8080/publication/950

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ZB-106436 Feb 4, 2023
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