Low-power helium:neon laser irradiation enhances production of vascular endothelial growth factor and promotes growth of endothelial cells in vitro

Background and Objective: Numerous reports suggest that low-power laser irradiation (LPLI) is capable of affecting cellular processes in the absence of significant thermal effect. The objective of the present study was to determine the effect of LPLI on secretion of vascular endothelial growth factor (VEGF) and proliferation of human endothelial cells (EC) in vitro. Study Design/Materials and Methods: Cell cultures were irradiated with single different doses of LPLI (Laser irradiance from 0.10 to 6.3 J/cm(2)) by using a He:Ne continuous wave laser (632 nm). VEGF secretion by smooth muscle cells (SMC) and fibroblasts was quantified by sandwich enzyme immunoassay technique. The endothelial cell proliferation was measured by Alamar Blue assay. VEGF and transforming growth factor beta (TGF-beta) expression by cardiomyocytes was studied by reverse transcription-polymerase chain reaction (RT-PCR). Results: We observed that (1) LPLI of vascular and cardiac cells results in a statistically significant increase of VEGF secretion in culture (1.6-fold for SMC and fibroblasts and 7-fold for cardiomyocytes) and is dose dependent (maximal effect was observed with LPLI irradiance of 0.5 J/cm(2) for SMC, 2.1 J/cm(2) for fibroblasts and 1.05 J/cm(2) for cardiomyocytes). (2) Significant stimulation of endothelial cell growth was obtained with LPLI-treated conditioned medium of SMC (maximal increase was observed with LPLI conditioned medium with irradiance of 1.05 J/ cm(2) for SMC and 2.1 J/cm(2) for fibroblasts. Conclusion: Our studies demonstrate that low-power laser irradiation increases production of VEGF by SMC, fibroblasts, and cardiac myocytes and stimulates EC growth in culture. These data may have significant importance leading to the establishment of new methods for endoluminal postangioplasty vascular repair and myocardial photoangiogenesis. Lasers Surg. Med. 28:355-364, 2001. (C) 2001 Wiley-Liss, Inc.