Loading…

Up‐regulation of Cartilage Oligomeric Matrix Protein Gene Expression by Insulin‐like Growth Factor‐I Revealed by Real Time Reverse Transcription‐Polymerase Chain Reaction

Cartilage oligomeric matrix protein (COMP) strengthens cartilage by binding to type II and type IX collagen‐forming bridges between collagen fibrils. It was hypothesized that perhaps one or more anabolic growth factors such as insulin‐like growth factor‐I (IGF‐I), fibroblast growth factor‐1 (FGF‐1)...

Full description

Saved in:
Bibliographic Details
Published in:Acta biochimica et biophysica Sinica 2006-10, Vol.38 (10), p.677-682
Main Authors: TIAN, Hua, STOGIANNIDIS, Ioannis
Format: Article
Language:English
Subjects:
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Cartilage oligomeric matrix protein (COMP) strengthens cartilage by binding to type II and type IX collagen‐forming bridges between collagen fibrils. It was hypothesized that perhaps one or more anabolic growth factors such as insulin‐like growth factor‐I (IGF‐I), fibroblast growth factor‐1 (FGF‐1) or platelet derived growth factor‐BB (PDGF‐BB) increase COMP gene expression. Their effects on primary human chondrocytes and the chondrogenic cell line ATDC5 were studied using real time reverse transcript‐polymerase chain reaction (RT‐PCR) for quantification. IGF‐I, but not the FGF‐1 or PDGF‐BB, up‐regulated COMP gene expression by approximate 5‐fold in human adult chondrocytes in a dose‐ and time‐dependent manner. IGF‐I exerted similar effects on ATDC5 cells. Results from these real time RT‐PCR experiments were confirmed by transfecting into ATDC5 cells a full‐length mouse COMP promoter cloned upstream of a luciferase reporter gene. On stimulation with IGF‐I, the luciferase reporter activity increased by about eight times. In conclusion, IGF‐I seems to be an important positive regulator of COMP, which may play an important role in an attempted repair of either traumatized or degenerated cartilage. Edited by Ming‐Hua XU
ISSN:1672-9145
1745-7270
DOI:10.1111/j.1745-7270.2006.00218.x