Abstract
Major facts about the development of restenosis include vascular smooth muscle cells (VSMCs) proliferation and migration. A previous study showed that in vitro treatment with magnesium chloride has the potential to affect the proliferation and migration of VSMCs. Magnesium is the major element in deep sea water (DSW) and is a biologically active mineral. It is unclear whether DSW intake can prevent abnormal proliferation and migration of VSMCs as well as balloon angioplasty-induced neointimal hyperplasia. Thus, we attempted to evaluate the anti-restenotic effects of DSW and its possible molecular mechanisms. Several concentrations of DSW, based on the dietary recommendations (RDA) for magnesium, were applied to a model of balloon angioplasty in SD rats. The results showed that DSW intake markedly increased magnesium content within the vascular wall and reduced the development of neointimal hyperplasia. The immunohistochemical analysis also showed that the expression of proteins associated with cell proliferation and migration were decreased in the balloon angioplasty groups with DSW supplement. Furthermore, in vitro treatment with DSW has a dose-dependent inhibitory effect on serum-stimulated proliferation and migration of VSMCs, whose effects might be mediated by modulation of mitogen-activated protein kinase (MAPK) signaling and of the activity of matrix metalloproteinase-2 (MMP-2). Our study suggested that DSW intake can help prevent neointimal hyperplasia (or restenosis), whose effects may be partially regulated by magnesium and other minerals.
Highlights
As a result of balloon injury-induced restenosis, vascular smooth muscle cells (VSMCs) predominantly undergoes proliferation and migration [1].The restenotic process is initiated by balloon angioplasty-induced vascular injury, which stimulates VSMCs to migrate from the medial layer to the intimal layer of the vessel wall and eventually results in uncontrolled neointimal hyperplasia
Our data showed that alkaline phosphatase (ALP) level was significantly increased on balloon angioplasty (BA) + water group, DSWtreated groups reversed the results (Table 1)
Our results shown no dramatic change of the serum Mg2+ concentration between DSWtreated and sham + water group (Table 1)
Summary
As a result of balloon injury-induced restenosis, VSMCs predominantly undergoes proliferation and migration [1].The restenotic process is initiated by balloon angioplasty-induced vascular injury, which stimulates VSMCs to migrate from the medial layer to the intimal layer of the vessel wall and eventually results in uncontrolled neointimal hyperplasia. The major problem of mineral deficiencies caused by the recent westernization of lifestyles and eating habits has resulted in so-called lifestyle-related illnesses such as coronary heart disease, angina pectoris, myocardial infarct, stroke, cancer, and diabetes [2,3]. Sternberg et al indicated that appropriate concentration of magnesium chloride has a potential in vitro effect to reduce cell viability of the primary VSMCs while increasing the viability of endothelial cells isolated from human coronary artery [6]. The experimental analysis from a cDNA microarray demonstrated that numerous genes for growth factors and their receptors, as well as for cell cycle and apoptosis-related signaling cascades, have been markedly up- or down regulated within these magnesium-chloride-treated VSMCs compared to those of endothelial cells [6]. Mg2+ deficiency might attribute to the development of hypertension, atherosclerosis, and other cardiovascular diseases (CVD)
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