Insulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytes

Yong Jun Wang, Qi Shi, Peng Sun, Quan Zhou, Michael Darowish, Tian Fang Li, Yu Feng Dong, William W. Lu, John C.Y. Leong

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Study Design. In vitro investigation of vertebral endplate chondrocyte apoptosis. Objectives. To determine whether Fas antibody caused apoptosis in endplate chondrocytes, and whether insulin-like growth factor-1 (IGF-1) inhibited this effect. Integrin-ā1 and focal adhesion kinase (FAK) expression in conjunction with apoptosis was also investigated. Summary of Background Data. Binding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects. Materials and Methods. Rat cervical endplate chondrocytes were cultured and treated with Fas antibody, with or without IGF-1. Cellular morphology was examined by microscopy. Apoptotic changes were evaluated by transmission electron microscopy, TUNEL staining, and immunostaining. Apoptosis-induced changes in the expression of integrin-ā1 chain and FAK were also investigated. Results. Endplate chondrocytes were able to be cultured; a chondrocytic phenotype was maintained. Fas antibody induced apoptosis in endplate chondrocytes; this was confirmed by TUNEL staining. Bcl-2 expression was decreased by Fas antibody, while Bax expression increased. Integrin-ā1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes. Conclusions. Fas antibody induces apoptosis and decreases Integrin-ā1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes.

Original languageEnglish (US)
Pages (from-to)736-741
Number of pages6
JournalSpine
Volume31
Issue number7
DOIs
StatePublished - Apr 1 2006

Fingerprint

Somatomedins
Chondrocytes
Focal Adhesion Kinase 1
Anti-Idiotypic Antibodies
Apoptosis
Antibodies
Integrins
In Situ Nick-End Labeling
Staining and Labeling
Transmission Electron Microscopy
Ligation
Microscopy
Phenotype

All Science Journal Classification (ASJC) codes

  • Orthopedics and Sports Medicine
  • Clinical Neurology

Cite this

Wang, Yong Jun ; Shi, Qi ; Sun, Peng ; Zhou, Quan ; Darowish, Michael ; Li, Tian Fang ; Dong, Yu Feng ; Lu, William W. ; Leong, John C.Y. / Insulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytes. In: Spine. 2006 ; Vol. 31, No. 7. pp. 736-741.
@article{fd5d7d93087a448290bc469e308bbdf9,
title = "Insulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytes",
abstract = "Study Design. In vitro investigation of vertebral endplate chondrocyte apoptosis. Objectives. To determine whether Fas antibody caused apoptosis in endplate chondrocytes, and whether insulin-like growth factor-1 (IGF-1) inhibited this effect. Integrin-ā1 and focal adhesion kinase (FAK) expression in conjunction with apoptosis was also investigated. Summary of Background Data. Binding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects. Materials and Methods. Rat cervical endplate chondrocytes were cultured and treated with Fas antibody, with or without IGF-1. Cellular morphology was examined by microscopy. Apoptotic changes were evaluated by transmission electron microscopy, TUNEL staining, and immunostaining. Apoptosis-induced changes in the expression of integrin-ā1 chain and FAK were also investigated. Results. Endplate chondrocytes were able to be cultured; a chondrocytic phenotype was maintained. Fas antibody induced apoptosis in endplate chondrocytes; this was confirmed by TUNEL staining. Bcl-2 expression was decreased by Fas antibody, while Bax expression increased. Integrin-ā1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes. Conclusions. Fas antibody induces apoptosis and decreases Integrin-ā1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes.",
author = "Wang, {Yong Jun} and Qi Shi and Peng Sun and Quan Zhou and Michael Darowish and Li, {Tian Fang} and Dong, {Yu Feng} and Lu, {William W.} and Leong, {John C.Y.}",
year = "2006",
month = "4",
day = "1",
doi = "10.1097/01.brs.0000208128.49912.64",
language = "English (US)",
volume = "31",
pages = "736--741",
journal = "Spine",
issn = "0362-2436",
publisher = "Lippincott Williams and Wilkins",
number = "7",

}

Insulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytes. / Wang, Yong Jun; Shi, Qi; Sun, Peng; Zhou, Quan; Darowish, Michael; Li, Tian Fang; Dong, Yu Feng; Lu, William W.; Leong, John C.Y.

In: Spine, Vol. 31, No. 7, 01.04.2006, p. 736-741.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Insulin-like growth factor-1 treatment prevents anti-fas antibody-induced apoptosis in endplate chondrocytes

AU - Wang, Yong Jun

AU - Shi, Qi

AU - Sun, Peng

AU - Zhou, Quan

AU - Darowish, Michael

AU - Li, Tian Fang

AU - Dong, Yu Feng

AU - Lu, William W.

AU - Leong, John C.Y.

PY - 2006/4/1

Y1 - 2006/4/1

N2 - Study Design. In vitro investigation of vertebral endplate chondrocyte apoptosis. Objectives. To determine whether Fas antibody caused apoptosis in endplate chondrocytes, and whether insulin-like growth factor-1 (IGF-1) inhibited this effect. Integrin-ā1 and focal adhesion kinase (FAK) expression in conjunction with apoptosis was also investigated. Summary of Background Data. Binding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects. Materials and Methods. Rat cervical endplate chondrocytes were cultured and treated with Fas antibody, with or without IGF-1. Cellular morphology was examined by microscopy. Apoptotic changes were evaluated by transmission electron microscopy, TUNEL staining, and immunostaining. Apoptosis-induced changes in the expression of integrin-ā1 chain and FAK were also investigated. Results. Endplate chondrocytes were able to be cultured; a chondrocytic phenotype was maintained. Fas antibody induced apoptosis in endplate chondrocytes; this was confirmed by TUNEL staining. Bcl-2 expression was decreased by Fas antibody, while Bax expression increased. Integrin-ā1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes. Conclusions. Fas antibody induces apoptosis and decreases Integrin-ā1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes.

AB - Study Design. In vitro investigation of vertebral endplate chondrocyte apoptosis. Objectives. To determine whether Fas antibody caused apoptosis in endplate chondrocytes, and whether insulin-like growth factor-1 (IGF-1) inhibited this effect. Integrin-ā1 and focal adhesion kinase (FAK) expression in conjunction with apoptosis was also investigated. Summary of Background Data. Binding of Fas antibody to Fas mimics Fas-FasL ligation, which causes apoptosis. IGF-1 has been shown to have anti-apoptotic effects. Materials and Methods. Rat cervical endplate chondrocytes were cultured and treated with Fas antibody, with or without IGF-1. Cellular morphology was examined by microscopy. Apoptotic changes were evaluated by transmission electron microscopy, TUNEL staining, and immunostaining. Apoptosis-induced changes in the expression of integrin-ā1 chain and FAK were also investigated. Results. Endplate chondrocytes were able to be cultured; a chondrocytic phenotype was maintained. Fas antibody induced apoptosis in endplate chondrocytes; this was confirmed by TUNEL staining. Bcl-2 expression was decreased by Fas antibody, while Bax expression increased. Integrin-ā1 and FAK expression was decreased by Fas antibody. IGF-1 treatment inhibited these Fas antibody-induced changes. Conclusions. Fas antibody induces apoptosis and decreases Integrin-ā1 and FAK expression in cultured endplate chondrocytes; IGF-1 is protective against these changes.

UR - http://www.scopus.com/inward/record.url?scp=33645797829&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33645797829&partnerID=8YFLogxK

U2 - 10.1097/01.brs.0000208128.49912.64

DO - 10.1097/01.brs.0000208128.49912.64

M3 - Article

C2 - 16582846

AN - SCOPUS:33645797829

VL - 31

SP - 736

EP - 741

JO - Spine

JF - Spine

SN - 0362-2436

IS - 7

ER -