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Targeting of focal adhesion kinase by small interfering RNAs reduces chondrocyte redifferentiation capacity in alginate beads culture with type II collagen

Authors
 YUN HEE KIM  ;  JIN WOO LEE 
Citation
 JOURNAL OF CELLULAR PHYSIOLOGY, Vol.218(3) : 623-630, 2009 
Journal Title
JOURNAL OF CELLULAR PHYSIOLOGY
ISSN
 0021-9541 
Issue Date
2009
MeSH
Adult ; Alginates/metabolism* ; Animals ; Cell Culture Techniques ; Cell Dedifferentiation ; Cell Differentiation* ; Cell Proliferation ; Cell Shape ; Chondrocytes/cytology* ; Chondrocytes/enzymology* ; Collagen Type II/metabolism* ; Enzyme Activation ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Focal Adhesion Protein-Tyrosine Kinases/metabolism* ; Gene Expression Regulation ; Glucuronic Acid/metabolism ; Glycosaminoglycans/metabolism ; Hexuronic Acids/metabolism ; Humans ; Microspheres ; Middle Aged ; Phosphorylation ; RNA, Small Interfering/metabolism* ; Smad Proteins/metabolism ; Swine
Abstract
Type II collagen is a major protein that maintains biological and mechanical characteristics in articular cartilage. Focal adhesion kinase (FAK) is known to play a central role in integrin signaling of cell-extracellular matrix (ECM) interactions, and chondrocyte-type II collagen interactions are very important for cartilage homeostasis. In this study, we focused on phosphorylation of FAK and MAP kinase in chondrocyte-type II collagen interaction and dedifferentiation, and the effects of FAK knockdown on chondrocyte-specific gene expression and cell proliferation were determined. The addition of exogenous type II collagen to chondrocytes increased levels of tyrosine phosphorylation, p-FAK(Y397), and p-ERK1/2. In contrast, expression levels of p-FAK(Y397) and p-ERK1/2, but not p-Smad2/3, were decreased in dedifferentiated chondrocytes with loss of type II collagen expression. Type II collagen expression was significantly increased when dedifferentiated chondrocytes were transferred to alginate beads with TGF-beta1 or type II collagen, but transfected cells with small interfering RNA for FAK (FAK-siRNA) inhibited mRNA expression of type II collagen and SOX-6 compared to the control. These FAK-siRNA-transfected cells could not recover type II collagen even in the presence of TGF-beta1 or type II collagen in alginate beads culture. We also found that FAK-siRNA-transfected cells decreased cell proliferation rate, but there was no effect on glycosaminoglycans (GAGs) secretion. We suggest that FAK is essentially required in chondrocyte communication with type II collagen by regulating type II collagen expression and cell proliferation.
Full Text
http://onlinelibrary.wiley.com/doi/10.1002/jcp.21637/abstract
DOI
10.1002/jcp.21637
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Orthopedic Surgery (정형외과학교실) > 1. Journal Papers
Yonsei Authors
Lee, Jin Woo(이진우) ORCID logo https://orcid.org/0000-0002-0293-9017
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/103443
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