Low-level laser irradiation modulates matrix metalloproteinase activity and gene expression in porcine aortic smooth muscle cells
Article first published online: 7 AUG 2006
Copyright © 2006 Wiley-Liss, Inc.
Lasers in Surgery and Medicine
Volume 38, Issue 8, pages 779–786, September 2006
How to Cite
Gavish, L., Perez, L. and Gertz, S. D. (2006), Low-level laser irradiation modulates matrix metalloproteinase activity and gene expression in porcine aortic smooth muscle cells. Lasers Surg. Med., 38: 779–786. doi: 10.1002/lsm.20383
- Issue published online: 19 SEP 2006
- Article first published online: 7 AUG 2006
- Manuscript Accepted: 8 JUN 2006
- Rachel and Barney Gotstein Research Fund
- Murray Koppelman Research Fund of the American Friends of the Hebrew University
- Anna and Arnold Broniatovsky Research Fund of the Hebrew University
- smooth muscle cell proliferation
Background and Objectives
The vascular extracellular matrix is maintained by a dynamic balance between matrix synthesis and degradation. This equilibrium is disrupted in arterial pathologies such as abdominal aortic aneurysm. Low-level laser irradiation (LLLI) promotes wound healing. However, its effect on smooth muscle cells (SMCs), a central player in these responses, has not been established. The current study was designed to determine the effects of LLLI on arterial SMC proliferation, inflammatory markers, and matrix proteins.
Study Design/Materials and Methods
Porcine primary aortic SMCs were irradiated with a 780 nm laser diode (1 and 2 J/cm2). Trypan blue exclusion assay, immunofluorescent staining for collagen I and III, Sircol assay, gelatin zymography, and RT-PCR were used to monitor proliferation; collagen trihelix formation; collagen synthesis; matrix metalloproteinase-2 (MMP-2) activity, and gene expression of MMP-1, MMP-2, tissue inhibitor of MMP-1 (TIMP-1), TIMP-2, and IL-1-β, respectively.
LLLI-increased SMC proliferation by 16 and 22% (1 and 2 J/cm2, respectively) compared to non-irradiated cells (P<0.01 and P<0.0005). Immediately after LLLI, trihelices of collagen I and III appeared as perinuclear fluorescent rings. Collagen synthesis was increased twofold (2 days after LLLI: 14.3±3.5 µg, non-irradiated control: 6.6±0.7 µg, and TGF-β stimulated control: 7.1±1.2 µg, P<0.05), MMP-2 activity after LLLI was augmented (over non-irradiated control) by 66±18% (2 J/cm2; P<0.05), and MMP-1 gene expression upregulated. However, TIMP-2 was upregulated, and MMP-2 gene expression downregulated. IL-1-β gene expression was reduced.
LLLI stimulates SMC proliferation, stimulates collagen synthesis, modulates the equilibrium between regulatory matrix remodeling enzymes, and inhibits pro-inflammatory IL-1-β gene expression. These findings may be of therapeutic relevance for arterial diseases such as aneurysm where SMC depletion, weakened extracellular matrix, and an increase in pro-inflammatory markers are major pathologic components. Lasers Surg. Med. 38:779–786, 2006. © 2006 Wiley-Liss, Inc.