Responsiveness to Retinoic Acid Changes during Chondrocyte Maturation

Iwamoto, Masahiro; Golden, Eleanor B.; Adams, Sherrill L.; Noji, Sumihare; Pacifici, Maurizio

doi:10.1006/excr.1993.1079

Cited by 77 publications

(68 citation statements)

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“…The immature chondrocytes of xiphoids in newborn mice have been shown to differ from other chondrocytes and become adipocytes under a defined in vitro condition (Heermeier et al, 1994). However, normal immature chondrocytes do not undergo adipogenesis, especially under the chondrocyte culture condition that we used in this study (Leboy et al, 1989;Iwamoto et al, 1993;Enomoto et al, 2000). The simultaneous induction of adipocyte differentiation and chondrocyte Journal of Cell Science 117 (3) differentiation in bone marrow cell cultures and mesenchymal cell line cultures is rare.…”

Section: Discussionmentioning

confidence: 85%

Runx2deficiency in chondrocytes causes adipogenic changes in vitro

Enomoto

Furuichi

Zanma

et al. 2004

Journal of Cell Science

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134

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Runx2 (runt-related transcription factor 2) is an important transcription factor for chondrocyte differentiation as well as for osteoblast differentiation. To investigate the function of Runx2 in chondrocytes, we isolated chondrocytes from the rib cartilage of Runx2-deficient (Runx2–/–) mice and examined the effect of Runx2 deficiency on chondrocyte function and behavior in culture for up to 12 days. At the beginning of the culture, Runx2–/– chondrocytes actively proliferated, had a polygonal shape and expressed type II collagen; these are all characteristics of chondrocytes. However, they gradually accumulated lipid droplets that stained with oil red O and resembled adipocytes. Northern blot analysis revealed that the expression of adipocyte-related differentiation marker genes including PPARγ (peroxisome proliferator-activated receptor γ), aP2 and Glut4 increased over time in culture, whereas expression of type II collagen decreased. Furthermore, the expression of Pref-1, an important inhibitory gene of adipogenesis, was remarkably decreased. Adenoviral introduction of Runx2 or treatment with transforming growth factor-β, retinoic acid, interleukin-1β, basic fibroblast growth factor, platelet-derived growth factor or parathyroid hormone inhibited the adipogenic changes in Runx2–/– chondrocytes. Runx2 and transforming growth factor-β synergistically upregulated interleukin-11 expression, and the addition of interleukin-11 to the culture medium reduced adipogenesis in Runx2–/– chondrocytes. These findings indicate that depletion of Runx2 resulted in the loss of the differentiated phenotype in chondrocytes and induced adipogenic differentiation in vitro, and show that Runx2 plays important roles in maintaining the chondrocyte phenotype and in inhibiting adipogenesis. Our findings suggest that these Runx2-dependent functions are mediated, at least in part, by interleukin-11.

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Section: Discussionmentioning

confidence: 85%

Runx2deficiency in chondrocytes causes adipogenic changes in vitro

Enomoto

Furuichi

Zanma

et al. 2004

Journal of Cell Science

Self Cite

134

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“…Chondrocytes were prepared from the caudal one-third portion of day-18 chicken embryo sterna as described previously (Iwamoto et al 1993;Kameda et al 1997;Watanabe et al 1997). They were purified by the elimination of fibroblastic cells through floating culture in DMEM containing 10% FCS for 5 days, and then treated with trypsin, and 80 000 cells were inoculated in 6 mm diameter stainless steel columns on collagencoated 60 mm tissue culture plates.…”

Section: Chondrocyte Culture and Virus Infectionmentioning

confidence: 99%

Developmental patterning in chondrocytic cultures by morphogenic gradients: BMP induces expression of Indian hedgehog and Noggin

et al. 1999

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“…In older cultured limb chondrocytes retinoids contribute to endochondral ossification and their maturation into hypertrophic cartilage. Accompanying their differentiation in response to retinoids is the characteristic loss of proteoglycans and collagen I1 and increases in collagen X, fibronectin, alkaline phosphatase, and perhaps collagen I (e.g., Solursh and Meier, 1973;Horton et al, 1987;Oettinger and Pacifici, 1990;Iwamoto et al, 1993). Retinoids may also stimulate chondrocytes into assuming an osteoblast phenotype (Gentile et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…The restriction of RARPl transcripts to the perichondrium suggests that this receptor might mediate some of these events. However, chick chondrocytes also express transcripts that cross-react with RARa and RARy (Pacifici et al, 1991;Iwamoto et al, 1993), so other contributors to these events are certainly likely.…”

Section: Discussionmentioning

confidence: 99%

Differential expression of retinoic acid receptor‐β isoforms during chick limb ontogeny

Smith

Kirstein

Wang

et al. 1995

Developmental Dynamics

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Retinoids influence both morphogenetic events and differentiation during development of the vertebrate limb. These effects are mediated through nuclear retinoid receptors, which modulate target gene expression. We report here the cloning and characterization of three promoter-and splicing-variants of the retinoic acid receptor-P (RAR-P) from chick. These receptor isoforms are independently expressed during limb development. RARp2 but not RARPl transcripts are enriched three-fold in the posterior limb bud, reflecting the increased RA concentrations in this region. RARPl transcripts are initially present throughout the limb bud mesenchyme and ectoderm, then become restricted within perichondrial regions and loose connective tissue of the limb. RARPl expression closely overlaps that of NCAM (neural cell adhesion molecule) and tenascin in non-neuronal tissues. RARP2 transcripts are present within a subset of those limb tissues which express RARP1. In the early limb bud RARP2 transcripts are detected in proximal limb mesenchyme and in the initial mesenchymal condensate. In older limbs RARP2 mRNAs are abundant in cells lateral to the digit cartilage. Neither RARPl nor RARP2 transcripts are associated specifically with regions of limb cell death. The differential expression and regulation of RARP isoforms suggests these variants may have different roles in limb development.

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Responsiveness to Retinoic Acid Changes during Chondrocyte Maturation

Cited by 77 publications

References 0 publications

Runx2deficiency in chondrocytes causes adipogenic changes in vitro

Runx2deficiency in chondrocytes causes adipogenic changes in vitro

Developmental patterning in chondrocytic cultures by morphogenic gradients: BMP induces expression of Indian hedgehog and Noggin

Differential expression of retinoic acid receptor‐β isoforms during chick limb ontogeny

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