Physiological role of vitamin a in growth cartilage cells: Low concentrations of retinoic acid strongly promote the proliferation of rabbit costal growth cartilage cells in culture

Motomi Enomoto, Haiou Pan, Fujio Suzuki, Masaharu Takigawa

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Abstract

We have demonstrated that high concentrations of retinoic acid (RA) inhibit expression of the differentiated phenotypes of rabbit costal chondrocytes in culture [M. Takigawa et al (1980) Proc. Natl. Acad. Sci. U. S. 77, 1481- 1485]. In this study we examined the effects of low concentrations of RA on rabbit costal chondrocytes cultured in medium containing vitamin A- deficient serum. In vitamin A- deficient medium, chondrocytes isolated from growth cartilage (GC) proliferated only very slowly, and RA strongly stimulated their proliferation. This stimulatory effect was observable at a concentration of 10- 10 M RA and maximal at a concentration of 10- 8 M. RA at 10- 8 M did not change GC cells from a typical polygonal shape to fibroblast-like cells or inhibit their synthesis of type II collagen. Moreover, RA-treated cells did not synthesize type I collagen. RA inhibited glycosamino-glycan (GAG) synthesis by the cells dose-dependently, but did not change the distribution profile of proteoglycan monomers as determined by glycerol gradient centrifugation. The inhibitory action of RA on GAG synthesis was reversible: after removal of RA from the culture, the rate of GAG synthesis increased within 2 days. In contrast, resting cartilage (RC) cells proliferated well in vitamin A- deficient medium without addition of RA, and RA (10- 8 M) stimulated their proliferation only slightly. Furthermore, the inhibitory effect of RA on GAG synthesis in RC cells was much weaker than that in GC cells. These observations suggest a physiological role of RA in cartilage in stimulating the proliferation of GC cells without causing drastic change in their differentiated phenotypes.

Original languageEnglish
Pages (from-to)743-748
Number of pages6
JournalJournal of Biochemistry
Volume107
Issue number5
Publication statusPublished - May 1990
Externally publishedYes

Fingerprint

Cartilage
Vitamins
Rabbit
Tretinoin
Proliferation
Cell Culture Techniques
Rabbits
Acids
Cell
Growth
Synthesis
Collagen
Polysaccharides
Phenotype
Chondrocytes
Vitamin A
Costal Cartilage
Culture
Fibroblasts
Dose

ASJC Scopus subject areas

  • Statistics, Probability and Uncertainty
  • Applied Mathematics
  • Physiology (medical)
  • Radiology Nuclear Medicine and imaging
  • Molecular Biology
  • Biochemistry

Cite this

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title = "Physiological role of vitamin a in growth cartilage cells: Low concentrations of retinoic acid strongly promote the proliferation of rabbit costal growth cartilage cells in culture",
abstract = "We have demonstrated that high concentrations of retinoic acid (RA) inhibit expression of the differentiated phenotypes of rabbit costal chondrocytes in culture [M. Takigawa et al (1980) Proc. Natl. Acad. Sci. U. S. 77, 1481- 1485]. In this study we examined the effects of low concentrations of RA on rabbit costal chondrocytes cultured in medium containing vitamin A- deficient serum. In vitamin A- deficient medium, chondrocytes isolated from growth cartilage (GC) proliferated only very slowly, and RA strongly stimulated their proliferation. This stimulatory effect was observable at a concentration of 10- 10 M RA and maximal at a concentration of 10- 8 M. RA at 10- 8 M did not change GC cells from a typical polygonal shape to fibroblast-like cells or inhibit their synthesis of type II collagen. Moreover, RA-treated cells did not synthesize type I collagen. RA inhibited glycosamino-glycan (GAG) synthesis by the cells dose-dependently, but did not change the distribution profile of proteoglycan monomers as determined by glycerol gradient centrifugation. The inhibitory action of RA on GAG synthesis was reversible: after removal of RA from the culture, the rate of GAG synthesis increased within 2 days. In contrast, resting cartilage (RC) cells proliferated well in vitamin A- deficient medium without addition of RA, and RA (10- 8 M) stimulated their proliferation only slightly. Furthermore, the inhibitory effect of RA on GAG synthesis in RC cells was much weaker than that in GC cells. These observations suggest a physiological role of RA in cartilage in stimulating the proliferation of GC cells without causing drastic change in their differentiated phenotypes.",
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T1 - Physiological role of vitamin a in growth cartilage cells

T2 - Low concentrations of retinoic acid strongly promote the proliferation of rabbit costal growth cartilage cells in culture

AU - Enomoto, Motomi

AU - Pan, Haiou

AU - Suzuki, Fujio

AU - Takigawa, Masaharu

PY - 1990/5

Y1 - 1990/5

N2 - We have demonstrated that high concentrations of retinoic acid (RA) inhibit expression of the differentiated phenotypes of rabbit costal chondrocytes in culture [M. Takigawa et al (1980) Proc. Natl. Acad. Sci. U. S. 77, 1481- 1485]. In this study we examined the effects of low concentrations of RA on rabbit costal chondrocytes cultured in medium containing vitamin A- deficient serum. In vitamin A- deficient medium, chondrocytes isolated from growth cartilage (GC) proliferated only very slowly, and RA strongly stimulated their proliferation. This stimulatory effect was observable at a concentration of 10- 10 M RA and maximal at a concentration of 10- 8 M. RA at 10- 8 M did not change GC cells from a typical polygonal shape to fibroblast-like cells or inhibit their synthesis of type II collagen. Moreover, RA-treated cells did not synthesize type I collagen. RA inhibited glycosamino-glycan (GAG) synthesis by the cells dose-dependently, but did not change the distribution profile of proteoglycan monomers as determined by glycerol gradient centrifugation. The inhibitory action of RA on GAG synthesis was reversible: after removal of RA from the culture, the rate of GAG synthesis increased within 2 days. In contrast, resting cartilage (RC) cells proliferated well in vitamin A- deficient medium without addition of RA, and RA (10- 8 M) stimulated their proliferation only slightly. Furthermore, the inhibitory effect of RA on GAG synthesis in RC cells was much weaker than that in GC cells. These observations suggest a physiological role of RA in cartilage in stimulating the proliferation of GC cells without causing drastic change in their differentiated phenotypes.

AB - We have demonstrated that high concentrations of retinoic acid (RA) inhibit expression of the differentiated phenotypes of rabbit costal chondrocytes in culture [M. Takigawa et al (1980) Proc. Natl. Acad. Sci. U. S. 77, 1481- 1485]. In this study we examined the effects of low concentrations of RA on rabbit costal chondrocytes cultured in medium containing vitamin A- deficient serum. In vitamin A- deficient medium, chondrocytes isolated from growth cartilage (GC) proliferated only very slowly, and RA strongly stimulated their proliferation. This stimulatory effect was observable at a concentration of 10- 10 M RA and maximal at a concentration of 10- 8 M. RA at 10- 8 M did not change GC cells from a typical polygonal shape to fibroblast-like cells or inhibit their synthesis of type II collagen. Moreover, RA-treated cells did not synthesize type I collagen. RA inhibited glycosamino-glycan (GAG) synthesis by the cells dose-dependently, but did not change the distribution profile of proteoglycan monomers as determined by glycerol gradient centrifugation. The inhibitory action of RA on GAG synthesis was reversible: after removal of RA from the culture, the rate of GAG synthesis increased within 2 days. In contrast, resting cartilage (RC) cells proliferated well in vitamin A- deficient medium without addition of RA, and RA (10- 8 M) stimulated their proliferation only slightly. Furthermore, the inhibitory effect of RA on GAG synthesis in RC cells was much weaker than that in GC cells. These observations suggest a physiological role of RA in cartilage in stimulating the proliferation of GC cells without causing drastic change in their differentiated phenotypes.

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