TITLE:
Effect of autologous mesenchymal stem cells induced by low level laser therapy on cardiogenesis in the infarcted area following myocardial infarction in rats
AUTHORS:
Hana Tuby, Tali Yaakobi, Lidya Maltz, Yaakov Delarea, Orit Sagi-Assif, Uri Oron
KEYWORDS:
Low-Level Laser Therapy; Myocardial Infarction; Macrophage; Desmin; Ultrastructure; c-Kit Positive Cells
JOURNAL NAME:
Journal of Biomedical Science and Engineering,
Vol.6 No.8A,
August
16,
2013
ABSTRACT: In this study, we investigated the hypothesis that photobiostimulation by low-energy laser therapy (LLLT) applied to the bone marrow (BM) of myocardial infarcted rats may attenuate the scarring processes that follow myocardial infarction (MI). Wistar rats underwent experimental MI. LLLT (Ga-Al-As diode laser) was applied to the BM of the exposed tibia at different time intervals post-MI (4 hrs, 48 hrs and 5 days). Sham-operated infarcted rats served as control. Infarct size was significantly reduced (55%) in the laser-treated rats as compared to the control non-treated rats, at 2 weeks post-MI. A significant 3-fold increase was observed in the density of desmin immunopositive stained cells 14 days post-MI in the infarcted area of the laser-treated rats as compared to the non-laser-treated controls. The electron microscopy from the control infarcted rat hearts revealed a typical interphase area between the intact myocardium and the infarcted area, with conspicuous fibroblasts with collagen deposition dispersed among them. In rats that were laser treated (to BM), the interphase zone demonstrated cells with different intracellular structures. There was also a significant increase in the percentage of c-kit positive cells and macrophages in the circulating blood of the laser treated rats as compared to control non treated ones. In the majority of the cells clusters of myofibrils anchored to well-developed Z-lines and structures resembling the morphological characteristics of mature intact cardiomyocytes were evident. In conclusion, LLLT to the BM of rats post-MI induces cardiogenesis mainly at the borders of the infarcted area in the heart.