title: The influence of vitamin D metabolites on the calcification of cartilage matrix and the C-propeptide of type II collagen (chondrocalcin).
abstract: The influence of vitamin D metabolites (at 1 X 10(-10) M) on the calcification of cartilage matrix (measured by 45Ca2+ uptake) and the C-propeptide of type II collagen (measured by radioimmunoassay) has been studied using organ cultures and chondrocytes isolated from growth plates of vitamin D-deficient and -sufficient 11-day-old rats. Vitamin D-deficient rats had reduced amounts of C-propeptide in their serum and freshly isolated growth plate chondrocytes. In all chondrocytes cultured from vitamin D-deficient animals, the C-propeptide content was maximal at 24 hr whereas calcification continued to increase for up to 72 hr. In organ and chondrocyte cultures of tissue from vitamin D-sufficient rats, both 1,25-dihydroxycholecalciferol (1,25(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25(OH)2D3) were required for maximal stimulation of calcification and maximal increases in C-propeptide content. In these D-replete tissues, 24,25-(OH)2D3 had a less stimulatory effect on both calcification (organ and cell cultures) and C-propeptide (organ cultures only), while 1,25(OH)2D3 alone had no effect in cell cultures but an inhibitory effect in organ cultures. Studies of cells or tissue from growth plates of vitamin D-deficient rats demonstrated that 24,25(OH)2D3 alone produced maximal calcification and maximal increases in the C-propeptide content. 1,25(OH)2D3 generally had an inhibitory effect on both calcification and C-propeptide when used alone. In the presence of 1,25(OH)2D3, the stimulatory effect of 24,25(OH)2D3 was partly abrogated. Maximal stimulation of calcification and increases in C-propeptide by 24,25(OH)2D3 were observed at 1 X 10(-9) M and 1 X 10(-10) M. In none of these studies was there any effect on proteoglycan content.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Shriners Hospital for Crippled Children, Department of Surgery, McGill University, Montreal, Quebec, Canada.
authors.forename: A
authors.initials: A
authors.lastname: Hinek
authors.forename: A R
authors.initials: AR
authors.lastname: Poole
mesh_terms: D015650:24,25-Dihydroxyvitamin D 3; D000818:Animals; D002113:Calcification, Physiologic / Q000187:drug effects*; D002117:Calcitriol / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000097:blood / Q000378:metabolism*; D002478:Cells, Cultured; D003094:Collagen / Q000097:blood / Q000378:metabolism*; D024043:Collagen Type II; D004100:Dihydroxycholecalciferols / Q000494:pharmacology*; D006132:Growth Plate / Q000187:drug effects / Q000502:physiology*; D009924:Organ Culture Techniques; D011498:Protein Precursors / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D014574:Uronic Acids / Q000032:analysis; D014808:Vitamin D Deficiency / Q000503:physiopathology*
chemical_list: D002135:Calcium-Binding Proteins; D024043:Collagen Type II; D004100:Dihydroxycholecalciferols; D011498:Protein Precursors; D014574:Uronic Acids; C040072:chondrocalcin; D015650:24,25-Dihydroxyvitamin D 3; D003094:Collagen; D002117:Calcitriol; D002118:Calcium