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Norepinephrine inhibits migration of human bone marrow mesenchymal stem cells
Author(s) -
Clark Kenneth,
Sepulveda Jorge L
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb115-b
Subject(s) - mesenchymal stem cell , stem cell , bone marrow , norepinephrine , in vivo , wound healing , in vitro , microbiology and biotechnology , cell migration , medicine , chemistry , endocrinology , biology , immunology , biochemistry , dopamine
Recent studies have shown that bone marrow mesenchymal stem cells (BM‐MSC's) may transdifferentiate into a cardiac phenotype, both in‐vitro and in‐vivo. Moreover, these cells appear to promote healing of injured myocardium, possibly by secreting cytokines and growth factors, which has implications for cellular therapy of various cardiac diseases, including myocardial infarction. It is not known, however, if and how mesenchymal stem cell migration is affected by systemic and locally produced catecholamines. Goal To study the effects of catecholamines on the migration of mesenchymal stem cells and elucidate the pathways by which these effects are manifested. Methods Immortalized human BM‐MSC's (AOC cells) were plated at 60–70% confluence in DMEM culture medium containing 10% fetal calf serum and a wound assay was performed to measure cellular migration. Norepinephrine was added to the wells and BM‐MSC migration was serially measured over the course of four days. Results After 4 days in culture, 0.1 mM norepinephrine had a statistically significant inhibitory effect on the migration of BM‐MSC's, with a reduction of almost 64% as compared to controls (p<0.0001). Conclusions Norepinephrine inhibits the migration of human mesenchymal stem cells in the presence of serum. Given the high tissue levels of cathecolamines in infarcted myocardium, these finding suggest a mechanism for local recruitment of BM‐MSC's with potential implications in the pathogenesis and treatment of myocardial disease.