Nongenomic Regulation of Protein Kinase C Isoforms by Vitamin D Metabolites in Chondrocyte Matrix Vesicles and Plasma Membranes.
Abstract
Normal biologic function of an organism requires communication and regulation at several levels. Perhaps the most fundamental communication is that which occurs between the extracellular matrix and the intracellular environment. Elucidation of the signal transduction pathways in the areas of chondrocyte, osteoblast and inflammatory regulation would have significant implications in wound healing, regenerative procedures, implants and treatment of metabolic diseases of bone and cartilage. The rat costochondral chondrocyte model has been used to demonstrate that vitamin D3 metabolites can directly regulate many cellular and extracellular matrix functions and that this regulation is dependent both on the type of vitamin D metabolite, and on the maturation level of the chondrocytes. Matrix vesicles, distinct extracellular organelles critically involved in matrix mineralization, are also differentially regulated by vitamin D metabolites. Recently, it was shown that vitamin D metabolites can regulate protein kinase C activity in chondrocyte culture lysates and that these effects are also metabolite- and maturation- specific. Protein kinase C (PKC) is a family of isozymes that are known to be important in cell signal transduction. The aim of this study was to examine whether PKC mediates the nongenomic effect of vitamin D on chondrocyte regulation. The present study investigated whether PKC activity was present in matrix vesicles (MV) and plasma membranes (PM) and whether this activity can be directly regulated by vitamin D metabolites. Rib cages from Sprague-Dawley rats were dissected to obtain resting zone (RC) and adjacent growth zone (CC) chondrocytes.
Document Details
- Document Type
- Technical Report
- Publication Date
- May 01, 1996
- Accession Number
- ADA320576
Entities
People
- Earl B. Ellis
Organizations
- Air Force Institute of Technology