Interaction of aortic endothelial and smooth muscle cells in culture Effect on glycosaminoglycan levels

Co-cultivation of various intra- and interspecific combinations of pig and rat aortic endothelial cells (AEC) and smooth muscle cells (SMC) resulted in a marked increase in hyaluronic acid (HA) levels, a smaller but significant increase in sulphated glycosaminoglycans (GAG), and an increase in the H...

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Published inAtherosclerosis Vol. 39; no. 2; pp. 147 - 161
Main Authors Merrilees, M.J., Scott, Lesley
Format Journal Article
LanguageEnglish
Published Ireland Elsevier Ireland Ltd 01.05.1981
Subjects
Animals
Aorta - cytology
Aorta - ultrastructure
Cell Communication
Cells, Cultured
Dermatan Sulfate
Endothelial cells
Endothelium - cytology
Endothelium - ultrastructure
Fibroblasts - ultrastructure
Glycosaminoglycans
HA/sulphated GAG ratio
Heparitin Sulfate
Hyaluronic Acid
Hyaluronic acid levels
Interaction in culture
Muscle, Smooth - cytology
Muscle, Smooth - ultrastructure
Rats
Smooth muscle cells
Swine
Glycosaminoglycans
Interaction in culture
Smooth muscle cells
HA/sulphated GAG ratio
Endothelial cells
Hyaluronic acid levels
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Summary:Co-cultivation of various intra- and interspecific combinations of pig and rat aortic endothelial cells (AEC) and smooth muscle cells (SMC) resulted in a marked increase in hyaluronic acid (HA) levels, a smaller but significant increase in sulphated glycosaminoglycans (GAG), and an increase in the HA/sulphated GAG ratio, compared with the separate culture of the two cell types. Culture of SMC in AEC-conditioned medium produced similar changes in GAG levels, whereas SMC-conditioned medium had no effect on AEC GAG levels. These results add further support for the concept that epithelial cells in general can modulate the GAG composition of adjacent connective tissue and thereby influence its morphological and physiological properties. It is suggested that the normal amounts, types and distribution of GAG in the arterial wall, and especially in the intima, may be partly dependent on interaction between the endothelium and SMC. It is further suggested that injury to endothelium, with a consequent failure in this interaction, could lead directly to changes in intimal GAG composition that contribute to lesion development.
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ISSN:0021-9150
1879-1484
DOI:10.1016/0021-9150(81)90064-2