Effects of tumor necrosis factor α on proliferation and expression of differentiated phenotypes in rabbit costal chondrocytes in culture

Motomi Enomoto, Hai Ou Pan, Akihiro Kinoshita, Yasutaka Yutani, Fujio Suzuki, Masaharu Takigawa

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Tumor necrosis factor α (TNFα) decreased the synthesis of glycosaminoglycan (GAG) in rabbit costal chondrocytes in culture, but did not stimulate the release of GAG from cell layers. Like chondrocytes cultured in control medium, chondrocytes cultured in the presence of TNFα produced putative "cartilage-specific" proteoglycans identified by density gradient centrifugation under dissociative conditions. Although TNFα decreased the synthesis of the proteoglycans, it did not change their monomeric size, which is a marker of cartilage phenotypes. Moreover, TNFα did not affect the responsiveness to parathyroid hormone, insulin-like growth factor I, or transforming growth factor β, which is known to stimulate GAG synthesis in cultured chondrocytes. TNFα decreased the alkaline phosphatase activity in the chondrocytes dose dependently. On the other hand, it stimulated their DNA synthesis slightly, but significantly. The stimulatory effect of TNFα on DNA synthesis was potentiated by fibroblast growth factor, epidermal growth factor, and fetal bovine serum. These findings suggest that in the presence of hormones and growth factors, TNFα promotes the proliferation of chondrocytes while suppressing their further differentiation at the stage of synthesis of cartilage-specific proteoglycans.

Original languageEnglish
Pages (from-to)145-151
Number of pages7
JournalCalcified Tissue International
Volume47
Issue number3
DOIs
Publication statusPublished - Sep 1990
Externally publishedYes

Fingerprint

Chondrocytes
Tumor Necrosis Factor-alpha
Rabbits
Phenotype
Proteoglycans
Glycosaminoglycans
Cartilage
Density Gradient Centrifugation
Fibroblast Growth Factors
DNA
Transforming Growth Factors
Parathyroid Hormone
Insulin-Like Growth Factor I
Epidermal Growth Factor
Alkaline Phosphatase
Intercellular Signaling Peptides and Proteins
Hormones
Serum

Keywords

  • Alkaline phosphatase
  • Chondrocytes
  • Proliferation
  • Proteoglycan
  • Tumor necrosis factor α

ASJC Scopus subject areas

  • Endocrinology
  • Orthopedics and Sports Medicine
  • Endocrinology, Diabetes and Metabolism

Cite this

Effects of tumor necrosis factor α on proliferation and expression of differentiated phenotypes in rabbit costal chondrocytes in culture. / Enomoto, Motomi; Pan, Hai Ou; Kinoshita, Akihiro; Yutani, Yasutaka; Suzuki, Fujio; Takigawa, Masaharu.

In: Calcified Tissue International, Vol. 47, No. 3, 09.1990, p. 145-151.

Research output: Contribution to journalArticle

Enomoto, Motomi ; Pan, Hai Ou ; Kinoshita, Akihiro ; Yutani, Yasutaka ; Suzuki, Fujio ; Takigawa, Masaharu. / Effects of tumor necrosis factor α on proliferation and expression of differentiated phenotypes in rabbit costal chondrocytes in culture. In: Calcified Tissue International. 1990 ; Vol. 47, No. 3. pp. 145-151.
@article{0d75cf4b07e2447daa58ce51fd6bb75a,
title = "Effects of tumor necrosis factor α on proliferation and expression of differentiated phenotypes in rabbit costal chondrocytes in culture",
abstract = "Tumor necrosis factor α (TNFα) decreased the synthesis of glycosaminoglycan (GAG) in rabbit costal chondrocytes in culture, but did not stimulate the release of GAG from cell layers. Like chondrocytes cultured in control medium, chondrocytes cultured in the presence of TNFα produced putative {"}cartilage-specific{"} proteoglycans identified by density gradient centrifugation under dissociative conditions. Although TNFα decreased the synthesis of the proteoglycans, it did not change their monomeric size, which is a marker of cartilage phenotypes. Moreover, TNFα did not affect the responsiveness to parathyroid hormone, insulin-like growth factor I, or transforming growth factor β, which is known to stimulate GAG synthesis in cultured chondrocytes. TNFα decreased the alkaline phosphatase activity in the chondrocytes dose dependently. On the other hand, it stimulated their DNA synthesis slightly, but significantly. The stimulatory effect of TNFα on DNA synthesis was potentiated by fibroblast growth factor, epidermal growth factor, and fetal bovine serum. These findings suggest that in the presence of hormones and growth factors, TNFα promotes the proliferation of chondrocytes while suppressing their further differentiation at the stage of synthesis of cartilage-specific proteoglycans.",
keywords = "Alkaline phosphatase, Chondrocytes, Proliferation, Proteoglycan, Tumor necrosis factor α",
author = "Motomi Enomoto and Pan, {Hai Ou} and Akihiro Kinoshita and Yasutaka Yutani and Fujio Suzuki and Masaharu Takigawa",
year = "1990",
month = "9",
doi = "10.1007/BF02555979",
language = "English",
volume = "47",
pages = "145--151",
journal = "Calcified Tissue International",
issn = "0171-967X",
publisher = "Springer New York",
number = "3",

}

TY - JOUR

T1 - Effects of tumor necrosis factor α on proliferation and expression of differentiated phenotypes in rabbit costal chondrocytes in culture

AU - Enomoto, Motomi

AU - Pan, Hai Ou

AU - Kinoshita, Akihiro

AU - Yutani, Yasutaka

AU - Suzuki, Fujio

AU - Takigawa, Masaharu

PY - 1990/9

Y1 - 1990/9

N2 - Tumor necrosis factor α (TNFα) decreased the synthesis of glycosaminoglycan (GAG) in rabbit costal chondrocytes in culture, but did not stimulate the release of GAG from cell layers. Like chondrocytes cultured in control medium, chondrocytes cultured in the presence of TNFα produced putative "cartilage-specific" proteoglycans identified by density gradient centrifugation under dissociative conditions. Although TNFα decreased the synthesis of the proteoglycans, it did not change their monomeric size, which is a marker of cartilage phenotypes. Moreover, TNFα did not affect the responsiveness to parathyroid hormone, insulin-like growth factor I, or transforming growth factor β, which is known to stimulate GAG synthesis in cultured chondrocytes. TNFα decreased the alkaline phosphatase activity in the chondrocytes dose dependently. On the other hand, it stimulated their DNA synthesis slightly, but significantly. The stimulatory effect of TNFα on DNA synthesis was potentiated by fibroblast growth factor, epidermal growth factor, and fetal bovine serum. These findings suggest that in the presence of hormones and growth factors, TNFα promotes the proliferation of chondrocytes while suppressing their further differentiation at the stage of synthesis of cartilage-specific proteoglycans.

AB - Tumor necrosis factor α (TNFα) decreased the synthesis of glycosaminoglycan (GAG) in rabbit costal chondrocytes in culture, but did not stimulate the release of GAG from cell layers. Like chondrocytes cultured in control medium, chondrocytes cultured in the presence of TNFα produced putative "cartilage-specific" proteoglycans identified by density gradient centrifugation under dissociative conditions. Although TNFα decreased the synthesis of the proteoglycans, it did not change their monomeric size, which is a marker of cartilage phenotypes. Moreover, TNFα did not affect the responsiveness to parathyroid hormone, insulin-like growth factor I, or transforming growth factor β, which is known to stimulate GAG synthesis in cultured chondrocytes. TNFα decreased the alkaline phosphatase activity in the chondrocytes dose dependently. On the other hand, it stimulated their DNA synthesis slightly, but significantly. The stimulatory effect of TNFα on DNA synthesis was potentiated by fibroblast growth factor, epidermal growth factor, and fetal bovine serum. These findings suggest that in the presence of hormones and growth factors, TNFα promotes the proliferation of chondrocytes while suppressing their further differentiation at the stage of synthesis of cartilage-specific proteoglycans.

KW - Alkaline phosphatase

KW - Chondrocytes

KW - Proliferation

KW - Proteoglycan

KW - Tumor necrosis factor α

UR - http://www.scopus.com/inward/record.url?scp=0025127783&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025127783&partnerID=8YFLogxK

U2 - 10.1007/BF02555979

DO - 10.1007/BF02555979

M3 - Article

C2 - 2224589

AN - SCOPUS:0025127783

VL - 47

SP - 145

EP - 151

JO - Calcified Tissue International

JF - Calcified Tissue International

SN - 0171-967X

IS - 3

ER -