Tags

Type your tag names separated by a space and hit enter

Targeting of focal adhesion kinase by small interfering RNAs reduces chondrocyte redifferentiation capacity in alginate beads culture with type II collagen.
J Cell Physiol. 2009 Mar; 218(3):623-30.JC

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.

Authors+Show Affiliations

Brain Korea 21 Project for Medical Sciences and Department of Orthopaedic Surgery, Yonsei University College of Medicine, Seoul, South Korea.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19006177

Citation

Kim, Yun Hee, and Jin Woo Lee. "Targeting of Focal Adhesion Kinase By Small Interfering RNAs Reduces Chondrocyte Redifferentiation Capacity in Alginate Beads Culture With Type II Collagen." Journal of Cellular Physiology, vol. 218, no. 3, 2009, pp. 623-30.
Kim YH, Lee JW. Targeting of focal adhesion kinase by small interfering RNAs reduces chondrocyte redifferentiation capacity in alginate beads culture with type II collagen. J Cell Physiol. 2009;218(3):623-30.
Kim, Y. H., & Lee, J. W. (2009). Targeting of focal adhesion kinase by small interfering RNAs reduces chondrocyte redifferentiation capacity in alginate beads culture with type II collagen. Journal of Cellular Physiology, 218(3), 623-30. https://doi.org/10.1002/jcp.21637
Kim YH, Lee JW. Targeting of Focal Adhesion Kinase By Small Interfering RNAs Reduces Chondrocyte Redifferentiation Capacity in Alginate Beads Culture With Type II Collagen. J Cell Physiol. 2009;218(3):623-30. PubMed PMID: 19006177.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeting of focal adhesion kinase by small interfering RNAs reduces chondrocyte redifferentiation capacity in alginate beads culture with type II collagen. AU - Kim,Yun Hee, AU - Lee,Jin Woo, PY - 2008/11/14/pubmed PY - 2009/1/14/medline PY - 2008/11/14/entrez SP - 623 EP - 30 JF - Journal of cellular physiology JO - J Cell Physiol VL - 218 IS - 3 N2 - 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. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/19006177/Targeting_of_focal_adhesion_kinase_by_small_interfering_RNAs_reduces_chondrocyte_redifferentiation_capacity_in_alginate_beads_culture_with_type_II_collagen_ L2 - https://doi.org/10.1002/jcp.21637 DB - PRIME DP - Unbound Medicine ER -