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Am J Physiol Heart Circ Physiol (April 7, 2006). doi:10.1152/ajpheart.00142.2006
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Submitted on February 7, 2006
Accepted on March 17, 2006

Cytokines Produced by Bone Marrow Cells can Contribute to Functional Improvement of the Infarcted Heart by Protecting Cardiomyocytes from Ischemic Injury

Masaya Takahashi1, Tao-Sheng Li2*, Ryo Suzuki1, Toshiro Kobayashi1, Hiroshi Ito1, Yasuhiro Ikeda2, Masunori Matsuzaki2, and Kimikazu Hamano1

1 Department of Surgery and Clinical Science, Yamaguchi University, Graduate School of Medicine, Ube, Japan
2 Department of Medical Bioregulation, Yamaguchi University School of Medicine, Ube, Japan

* To whom correspondence should be addressed. E-mail: litaoshe{at}yamaguchi-u.ac.jp.

It is well known that the implantation of bone marrow mononuclear cells (BM-MNCs) into ischemic hearts can induce angiogenesis and improve cardiac function after myocardial infarction, but the precise mechanisms of these actions are unclear. We hypothesize that the cytokines produced by BM-MNCs play a key role in this cell-based therapy. BM-MNCs from rats were cultured under normoxic or hypoxic (1% O2) conditions for 24 hours, and then supernatants were collected for study. ELISA and Western blotting analysis showed that various cytokines, including vascular endothelial growth factor, interleukin-1beta, platelet-derived growth factor, and insulin-like growth factor 1, were produced from BM-MNCs, some of which were enhanced significantly under hypoxia stimulation. Compared with a control blank medium, the supernatants of BM-MNCs cultured under normoxic or hypoxic conditions inhibited apoptosis significantly, and preserved the contractile capacity of isolated adult rat cardiomyocytes in vitro (p<0.05). Using a rat model of acute myocardial infarction, we injected the supernatants of BM-MNCs or control medium intramyocardially on day 0, and then intraperitoneally on days 2, 4, and 6 after infarction. Compared with the control medium, the supernatants of BM-MNCs cultured under both normoxic or hypoxic conditions increased the microvessel density and decreased the fibrotic area in the infarcted myocardium significantly, contributing to remarkable improvement in cardiac function. Various cytokines were produced by BM-MNCs, and these cytokines contributed to functional improvement of the infarcted heart by directly preserving the contractile capacity of the myocardium, inhibiting apoptosis of cardiomyocytes, and inducing therapeutic angiogenesis of the infarcted heart.




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