## Abstract Hyaluronan (or hyaluronic acid, HA) is an essential component of extracellular matrices. It interacts with other macromolecules and plays a predominant role in tissue morphogenesis, cell migration, differentiation, and adhesion. The cell signaling functions of HA are mediated through th
Microvessel endothelial cells and pericytes increase proliferation and repress osteoblast phenotypic markers in rat calvarial bone cell cultures
✍ Scribed by A. R. Jones; C. C. Clark; C. T. Brighton
- Publisher
- Elsevier Science
- Year
- 1995
- Tongue
- English
- Weight
- 1011 KB
- Volume
- 13
- Category
- Article
- ISSN
- 0736-0266
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✦ Synopsis
Abstract
To investigate the influence of microvessel cells on osteoblasts, we exposed osteoblast‐enriched cultures of rat calvarial cells to cultured endothelial cells and pericytes using feeder‐layer co‐cultures, co‐culture dish inserts, and conditioned media experiments. When co‐cultured with growth‐arrested feeder‐layers of endothelial cells or pericytes for 10 days, bone cell cultures showed an increase in cell number and reduction in alkaline phosphatase activity. The response of bone cells to endothelial cells was nearly twice their response to pericytes. A similar response was demonstrated by exposure to microvessel cells in co‐culture dish inserts and by exposure to media conditioned by microvessel cells. In long‐term cultures of bone cells, the levels of osteocalcin and the number of mineralized nodules both were reduced by exposure to media conditioned by the microvessel cells. Transient exposure to conditioned media from the microvessel cell cultures for 3 days, during the period from initial plating to cell confluence, produced nearly the same effect on the cultures of bone cells as did continuous exposure to these conditioned media. The influence of isolated microvessel cells on osteoblast‐enriched calvarial cells was found to be primarily mitogenic, mediated by soluble factors, independent of cell contact, and a cause of prolonged reduction in the expression of early and late markers of the osteoblast phenotype.
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During bone loss, osteoblast population can be replaced by adipose tissue. This apparent reciprocal relationship between decreased bone density and increased fat formation can be explained by an imbalance in the production of bone-forming and fat-forming cells in the marrow cavity. Thus, osteoblast