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Enhanced proliferation of aortal smooth muscle cells treated by 1,25(OH) 2 D 3 in vitro coincides with impaired formation of elastic fibres
Author(s) -
Tukaj Cecylia
Publication year - 2008
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.1365-2613.2008.00578.x
Subject(s) - elastin , calcitriol , extracellular matrix , vascular smooth muscle , in vitro , chemistry , ultrastructure , extracellular , cell growth , microbiology and biotechnology , matrix (chemical analysis) , biophysics , endocrinology , biology , anatomy , smooth muscle , vitamin d and neurology , biochemistry , genetics , chromatography
Summary Elastin is the major extracellular matrix component synthesized, secreted and deposited by vascular smooth muscle cells (SMCs) in the arterial media and thus plays an important role in vascular homeostasis. Results of our previous studies showed that 1α,25‐dihydroxycholecalciferol [1,25(OH) 2 D 3 ‐calcitriol] accelerates proliferation of SMCs and modulates their growth in vitro . The aim of this study was to find ultrastructural support for the idea that 1,25(OH) 2 D 3 ‐calcitriol affects elastic fibre formation due to accelerated proliferation of aortal SMCs in vitro . SMCs exposed 10 days to supraphysiological concentration (10 nM) of calcitriol in primary culture were examined by fluorescence and transmission electron microscopy. Morphological studies revealed that calcitriol altered elastin maturation by favouring accumulation of immature rather than fully processed elastic fibres. A substantial decrease in the amorphous elastin deposition and abnormal accumulation of microfibrillar component, in thickened multilayer culture, were observed. These studies suggest that 1,25(OH) 2 D 3 affect formation of elastic fibres due to enhanced proliferation of SMCs in culture.