Modulation of commitment, proliferation, and differentiation of chondrogenic cells in defined culture medium

Rodolfo Quarto, Giuliano Campanile, Ranieri Cancedda, Beatrice Dozin

Research output: Contribution to journalArticle

72 Citations (Scopus)

Abstract

The factors regulating the growth and development of mesenchymal precursor cells toward chondrogenesis are not well identified. We have developed a defined serum-free culture system that allows the proliferation of chick embryo chondrogenic cells and their maturation toward hypertrophic chondrocytes. Proliferation is obtained in adhesion in medium supplemented with insulin (Ins), Dexamethasone (Dex), and either basic fibroblast growth factor (FGF-2), platelet-derived growth factor bb, epithelial growth factor, or GH; the highest mitogenic response is induced by FGF-2 in synergy with Ins. Ins can be substituted by Ins-like growth factor I. When these cells are transferred into suspension culture in Ins/Dex and T3 without growth factor supplement, they undergo the complete chondrogenic development characterized by type X collagen synthesis and cellular hypertrophy. During differentiation, Ins cannot be substituted by Ins-like growth factor I. Chondrogenesis is also evidenced by the formation of hypertrophic cartilage when the medium is supplemented with ascorbic acid. If T3 is introduced in the proliferation phase, the cells fail to differentiate to hypertrophy in suspension unless bone morphogenetic protein-2 is added. Assays ectopic tissue formation in nude mice, with cells implanted sc after adsorption on collagen sponge or porous hydroxyapatite ceramics, indicate that cells grown in Ins/FGF-2 reform mainly cartilage in vivo, whereas expansion in Ins/T3Dex/FGF-2 leads to the formation of cartilage, bone, and adipose tissue.

Original languageEnglish
Pages (from-to)4966-4976
Number of pages11
JournalEndocrinology
Volume138
Issue number11
DOIs
Publication statusPublished - 1997

Fingerprint

Fibroblast Growth Factor 2
Culture Media
Cell Differentiation
Insulin
Cartilage
Chondrogenesis
Insulin-Like Growth Factor I
Hypertrophy
Dexamethasone
Intercellular Signaling Peptides and Proteins
Suspensions
Collagen Type X
Choristoma
Bone Morphogenetic Protein 2
Platelet-Derived Growth Factor
Ceramics
Porifera
Chick Embryo
Durapatite
Chondrocytes

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Modulation of commitment, proliferation, and differentiation of chondrogenic cells in defined culture medium. / Quarto, Rodolfo; Campanile, Giuliano; Cancedda, Ranieri; Dozin, Beatrice.

In: Endocrinology, Vol. 138, No. 11, 1997, p. 4966-4976.

Research output: Contribution to journalArticle

@article{7a209729f0554b3c85e66b4924446b84,
title = "Modulation of commitment, proliferation, and differentiation of chondrogenic cells in defined culture medium",
abstract = "The factors regulating the growth and development of mesenchymal precursor cells toward chondrogenesis are not well identified. We have developed a defined serum-free culture system that allows the proliferation of chick embryo chondrogenic cells and their maturation toward hypertrophic chondrocytes. Proliferation is obtained in adhesion in medium supplemented with insulin (Ins), Dexamethasone (Dex), and either basic fibroblast growth factor (FGF-2), platelet-derived growth factor bb, epithelial growth factor, or GH; the highest mitogenic response is induced by FGF-2 in synergy with Ins. Ins can be substituted by Ins-like growth factor I. When these cells are transferred into suspension culture in Ins/Dex and T3 without growth factor supplement, they undergo the complete chondrogenic development characterized by type X collagen synthesis and cellular hypertrophy. During differentiation, Ins cannot be substituted by Ins-like growth factor I. Chondrogenesis is also evidenced by the formation of hypertrophic cartilage when the medium is supplemented with ascorbic acid. If T3 is introduced in the proliferation phase, the cells fail to differentiate to hypertrophy in suspension unless bone morphogenetic protein-2 is added. Assays ectopic tissue formation in nude mice, with cells implanted sc after adsorption on collagen sponge or porous hydroxyapatite ceramics, indicate that cells grown in Ins/FGF-2 reform mainly cartilage in vivo, whereas expansion in Ins/T3Dex/FGF-2 leads to the formation of cartilage, bone, and adipose tissue.",
author = "Rodolfo Quarto and Giuliano Campanile and Ranieri Cancedda and Beatrice Dozin",
year = "1997",
doi = "10.1210/en.138.11.4966",
language = "English",
volume = "138",
pages = "4966--4976",
journal = "Endocrinology",
issn = "0013-7227",
publisher = "The Endocrine Society",
number = "11",

}

TY - JOUR

T1 - Modulation of commitment, proliferation, and differentiation of chondrogenic cells in defined culture medium

AU - Quarto, Rodolfo

AU - Campanile, Giuliano

AU - Cancedda, Ranieri

AU - Dozin, Beatrice

PY - 1997

Y1 - 1997

N2 - The factors regulating the growth and development of mesenchymal precursor cells toward chondrogenesis are not well identified. We have developed a defined serum-free culture system that allows the proliferation of chick embryo chondrogenic cells and their maturation toward hypertrophic chondrocytes. Proliferation is obtained in adhesion in medium supplemented with insulin (Ins), Dexamethasone (Dex), and either basic fibroblast growth factor (FGF-2), platelet-derived growth factor bb, epithelial growth factor, or GH; the highest mitogenic response is induced by FGF-2 in synergy with Ins. Ins can be substituted by Ins-like growth factor I. When these cells are transferred into suspension culture in Ins/Dex and T3 without growth factor supplement, they undergo the complete chondrogenic development characterized by type X collagen synthesis and cellular hypertrophy. During differentiation, Ins cannot be substituted by Ins-like growth factor I. Chondrogenesis is also evidenced by the formation of hypertrophic cartilage when the medium is supplemented with ascorbic acid. If T3 is introduced in the proliferation phase, the cells fail to differentiate to hypertrophy in suspension unless bone morphogenetic protein-2 is added. Assays ectopic tissue formation in nude mice, with cells implanted sc after adsorption on collagen sponge or porous hydroxyapatite ceramics, indicate that cells grown in Ins/FGF-2 reform mainly cartilage in vivo, whereas expansion in Ins/T3Dex/FGF-2 leads to the formation of cartilage, bone, and adipose tissue.

AB - The factors regulating the growth and development of mesenchymal precursor cells toward chondrogenesis are not well identified. We have developed a defined serum-free culture system that allows the proliferation of chick embryo chondrogenic cells and their maturation toward hypertrophic chondrocytes. Proliferation is obtained in adhesion in medium supplemented with insulin (Ins), Dexamethasone (Dex), and either basic fibroblast growth factor (FGF-2), platelet-derived growth factor bb, epithelial growth factor, or GH; the highest mitogenic response is induced by FGF-2 in synergy with Ins. Ins can be substituted by Ins-like growth factor I. When these cells are transferred into suspension culture in Ins/Dex and T3 without growth factor supplement, they undergo the complete chondrogenic development characterized by type X collagen synthesis and cellular hypertrophy. During differentiation, Ins cannot be substituted by Ins-like growth factor I. Chondrogenesis is also evidenced by the formation of hypertrophic cartilage when the medium is supplemented with ascorbic acid. If T3 is introduced in the proliferation phase, the cells fail to differentiate to hypertrophy in suspension unless bone morphogenetic protein-2 is added. Assays ectopic tissue formation in nude mice, with cells implanted sc after adsorption on collagen sponge or porous hydroxyapatite ceramics, indicate that cells grown in Ins/FGF-2 reform mainly cartilage in vivo, whereas expansion in Ins/T3Dex/FGF-2 leads to the formation of cartilage, bone, and adipose tissue.

UR - http://www.scopus.com/inward/record.url?scp=0030778821&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030778821&partnerID=8YFLogxK

U2 - 10.1210/en.138.11.4966

DO - 10.1210/en.138.11.4966

M3 - Article

C2 - 9348228

AN - SCOPUS:0030778821

VL - 138

SP - 4966

EP - 4976

JO - Endocrinology

JF - Endocrinology

SN - 0013-7227

IS - 11

ER -