The Modulation of Integrin Expression by the Extracellular Matrix in Articular Chondrocytes.
10.3349/ymj.2003.44.3.493
- Author:
Sung Jae KIM
1
;
Eun Jung KIM
;
Yun Hee KIM
;
Soo Bong HAHN
;
Jin Woo LEE
Author Information
1. Department of Orthopaedic Surgery, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul 120-752, Korea. ljwos@yumc.yonsei.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Articular chondrocyte;
integrin;
extracellular matrix;
alginate culture;
monolayer culture
- MeSH:
Animals;
Cartilage, Articular/cytology/*metabolism;
Chondrocytes/*metabolism;
Extracellular Matrix/*physiology;
Fluorescent Antibody Technique;
Integrins/genetics/*metabolism;
Reverse Transcriptase Polymerase Chain Reaction;
Support, Non-U.S. Gov't;
Swine
- From:Yonsei Medical Journal
2003;44(3):493-501
- CountryRepublic of Korea
- Language:English
-
Abstract:
Normal articular cartilage is composed of chondrocytes embedded within an extracellular matrix (ECM). The patterns of integrin expression determine the adhesive properties of cells by modulating interactions with specific ECMs. Our hypothesis is that chondrocyte integrin expression changes in response to changes in their microenvironment. Porcine articular chondrocytes were encapsulated in alginate beads with several ECMs (collagen type I, collagen type II and fibronectin) for 7 days, subjected to RT-PCR, western blot analysis and immunofluorescence staining. It was found that chondrocytes in different ECMs showed different patterns of integrin expression. Integrin alpha5 and beta1 were strongly expressed in all groups, but integrin alpha1 was strongly expressed only in collagen type I and fibronectin conjugated alginate beads, and integrin alpha2 was strongly expressed only in collagen type II conjugated alginate beads. These findings suggest that the addition of different ECMs to chondrocytes can modulate the patterns and levels of integrin expression possibly through a feedback mechanism. These finding suggest that the modulation of ECM interactions may play a critical role in the pathogenesis of osteoarthritis.
