Vitamin A, Sulfation and Bone Growth in the Chick

Havivi, E; Wolf, George

doi:10.1093/jn/92.4.467

Cited by 28 publications

(4 citation statements)

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“…In contrast, in vitamin A deficiency (hypovitaminosis A), the growth plate has an ill-defined, immature proliferative zone with few mitotic figures [Wolbach and Hegsted, 1952;Howell and Thompson, 1967] as well as a narrow, undercalcified maturation-hypertrophic zone. In addi-tion, there is an abundant proteoglycan-rich extracellular matrix and reduced vascular invasion of the hypertrophic zone [Howell and Thompson, 1967;Havivi and Wolf, 1967].…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid treatment elevates matrix metalloproteinase-2 protein and mRNA levels in avian growth plate chondrocyte cultures

et al. 1998

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Matrix metalloproteinases (MMPs) play a crucial role in tissue remodeling. In growth plate (GP) cartilage, extensive remodeling occurs at the calcification front. To study the potential involvement of MMPs in retinoic acid (RA) regulation of skeletal development, we studied the effect of all-trans-RA on MMPs levels in mineralizing chicken epiphyseal chondrocyte primary cultures. When treated for 4 day periods on days 10 and 17, RA increased levels of an approximately 70 kDa gelatinase activity. The N-terminal sequence of the first 20 amino acid residues of the purified enzyme was identical to that deduced from chicken MMP-2 cDNA. Time-course studies indicated that RA elevated MMP-2 activity levels in the cultures within 16 h. This increase was inhibited by cycloheximide and was enhanced by forskolin. The increase in MMP-2 activity induced by RA was accompanied by an increase in MMP-2 mRNA levels and was abolished by treatment with cycloheximide. This upregulation of MMP levels by RA in GP chondrocytes is consistent with its effects on osteoblasts and osteosarcoma cells and opposite its inhibitory effects on fibroblasts and endothelial cells. It may well be related to the breakdown of the extracellular matrix in the GP and would be governed by the availability of RA at the calcification front where extensive vascularization also occurs.

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Section: Discussionmentioning

confidence: 99%

Retinoic acid treatment elevates matrix metalloproteinase-2 protein and mRNA levels in avian growth plate chondrocyte cultures

et al. 1998

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“…In pregnant animals, both hypovitaminosis A and hypervitaminosis A cause severe skeletal alterations in the developing fetus. In hypovitaminosis A, the growth plate contains an ill-defined proliferative area with very few mitotic figures; in addition, the hypertrophic zone is narrow and hypomineralized, and vascular invasion is markedly reduced (Havivi and Wolf, 1967;Howell and Thompson, 1967;Wolbach and Hegsted, 1952). In contrast, in hypervitaminosis A, the growth plate contains a wide hypertrophic area, which undergoes precocious mineralization and vascular invasion; this process is associated with premature involution and closure of the growth plate (Vasan and Lash, 1975;Wolbach and Hegsted, 1953).…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid is a major regulator of chondrocyte maturation and matrix mineralization

Iwamoto

Yagami

Shapiro

et al. 1994

Microscopy Res & Technique

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During the process of endochondral bone formation, chondrocytes undergo a series of complex maturational changes. Our recent studies indicate that this maturational process is influenced by the vitamin A derivative retinoic acid (RA). To learn how this agent regulates chondrocyte development, we characterized matrix gene expression during maturation of cartilage cells in chick sternum. RNAs were isolated from the cephalic portion of day 13, 14, 16, 18, and 20 chick embryo sternum and analyzed via northern blots. Type II collagen RNA levels remained fairly constant during this developmental period. In contrast, expression of type X collagen and alkaline phosphatase (APase) genes was first detected at day 16, followed by that of osteonectin (ON) and osteopontin (OP). To explore the mechanisms triggering these changes, chondrocytes were isolated from the cephalic portion of day 17-18 sternum (US cells) and grown in monolayer in standard serum-containing medium. After 3 weeks in culture, most of the cells enlarged and became type X collagen-positive, but they exhibited low APase activity and contained only trace amounts of ON and OP mRNAs. Treatment of parallel 3-week-old cultures with RA (10-100 nM) rapidly increased expression of the APase, ON, and OP genes severalfold. In concert with a significant increase in APase activity, there was abundant calcium accumulation in the RA-treated cultures. Electron microscopy confirmed the formation of large matrix-associated mineral crystals and the presence of numerous matrix vesicles. The effects of RA were also studied in cultures of immature chondrocytes isolated from the caudal portion of sternum (LS cells).(ABSTRACT TRUNCATED AT 250 WORDS)

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“…In hypervitaminosis A, a narrow proliferative zone and a wide hyper-trophic zone are present in growth plate cartilage; in addition, precocious matrix mineralization and vascular invasion are obvious [Wolbach and Hegsted, 1953;Vasan and Lash, 1975]. In vitamin A deficiency (hypovitaminosis A), the growth plate has an ill-defined immature proliferative zone with little mitotic activity, and a narrow, undercalcified maturation/hypertrophic zone; however, there is an abundant proteoglycan (PG)-rich extracellular matrix [Howell and Thompson, 1967;Havivi and Wolf, 1967].…”

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confidence: 99%

Retinoic acid stimulates matrix calcification and initiates type I collagen synthesis in primary cultures of avian weight-bearing growth plate chondrocytes

Ishikawa

Nie

et al. 1997

J. Cell. Biochem.

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The effect of retinoic acid (RA) on primary cultures of growth plate chondrocytes obtained from weight-bearing joints was examined, Chondrocytes were isolated from the tibial epiphysis of 6- to 8-week-old broiler-strain chickens and cultured in either serum-containing or serum-free media. RA was administered at low levels either transiently or continuously after the cells had become established in culture. Effects of RA on cellular protein levels, alkaline phosphatase (AP) activity, synthesis of proteoglycan (PG), matrix calcification, cellular morphology, synthesis of tissue-specific types of collagen, and level of matrix metalloproteinase (MMP) activity were explored. RA treatment generally increased AP activity and stimulated mineral deposition, especially if present continuously. RA also caused a shift in cell morphology from spherical/polygonal to spindle-like. This occurred in conjunction with a change in the type of collagen synthesized: type X and II collagens were decreased, while synthesis of type I collagen was increased. There was also a marked increase in the activity of MMP. Contrasting effects of continuous RA treatment on cellular protein levels were seen: they were enhanced in serum-containing media, but decreased in serum-free HL-1 media. Levels of RA as low as 10 nM significantly inhibited PG synthesis and caused depletion in the levels of PG in the medium and cell-matrix layer. Thus, in these appendicular chondrocytes, RA suppressed chondrocytic (PG, cartilage-specific collagens) and enhanced osteoblastic phenotype (cell morphology, type I collagen, alkaline phosphatase, and mineralization).

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Vitamin A, Sulfation and Bone Growth in the Chick

Cited by 28 publications

References 0 publications

Retinoic acid treatment elevates matrix metalloproteinase-2 protein and mRNA levels in avian growth plate chondrocyte cultures

Retinoic acid treatment elevates matrix metalloproteinase-2 protein and mRNA levels in avian growth plate chondrocyte cultures

Retinoic acid is a major regulator of chondrocyte maturation and matrix mineralization

Retinoic acid stimulates matrix calcification and initiates type I collagen synthesis in primary cultures of avian weight-bearing growth plate chondrocytes

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