Open AccessEthanol increases phosphate‐mediated mineralization and osteoblastic transformation of vascular smooth muscle cells
Author(s) -
Oros Melinda,
Zavaczki Erzsebet,
Vadasz Csaba,
Jeney Viktoria,
Tosaki Arpad,
Lekli Istvan,
Balla Gyorgy,
Nagy Laszlo,
Balla Jozsef
Publication year - 2012
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2012.01533.x
Subject(s) - vascular smooth muscle , mineralization (soil science) , phosphate , ethanol , chemistry , microbiology and biotechnology , smooth muscle , medicine , endocrinology , biochemistry , biology , organic chemistry , nitrogen
Abstract Vascular calcification is implicated in the pathogenesis of atherosclerosis, diabetes and chronic kidney disease. Human vascular smooth muscle cells ( HSMCs ) undergo mineralization in response to elevated levels of inorganic phosphate ( Pi ) in an active and well‐regulated process. This process involves increased activity of alkaline phosphatase and increased expression of core binding factor α‐1 ( CBF‐α1 ), a bone‐specific transcription factor, with the subsequent induction of osteocalcin. It has been shown that heavy alcohol consumption is associated with greater calcification in coronary arteries. The goal of our study was to examine whether ethanol alters mineralization of HSMCs provoked by high Pi. Exposure of HSMCs to ethanol increased extracellular matrix calcification in a dose responsive manner, providing a significant additional calcium deposition at concentrations of ≥60 mmol/l. HSMC calcification was accompanied by further enhancement in alkaline phosphatase activity. Ethanol also provoked a significant increase in the synthesis of osteocalcin. Moreover, in cells challenged with ethanol the expression of CBF‐α1 , a transcription factor involved in the regulation of osteoblastic transformation of HSMCs , was elevated. The observed effects of ethanol were not due to alterations of phosphate uptake by HSMCs . We conclude that ethanol enhances P i‐mediated human vascular smooth muscle calcification and transition of these cells into osteoblast‐like cells.