Overexpression of SOX9 in mouse embryonic stem cells directs the immediate chondrogenic commitment.
- Author:
Jae Hwan KIM
1
;
Hyun Jin DO
;
Heung Mo YANG
;
Jong Hyun OH
;
Seong Jun CHOI
;
Dong Ku KIM
;
Kwang Yul CHA
;
Hyung Min CHUNG
Author Information
1. Cell and Gene Therapy Research Institute.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
cell differentiation;
chondrogenesis;
sox9;
transcription factor;
stem cells;
transfection
- MeSH:
Animals;
Cell Differentiation/genetics;
Cell Line;
*Chondrogenesis;
Collagen Type II/genetics;
Embryo/*cytology;
Enhancer Elements (Genetics)/genetics;
Extracellular Matrix Proteins/genetics;
Genetic Markers/genetics;
High Mobility Group Proteins/genetics/*metabolism;
Humans;
Lectins, C-Type/genetics;
Mice;
Paired Box Transcription Factors/genetics;
Proteoglycans/genetics;
Research Support, Non-U.S. Gov't;
Stem Cells/*metabolism/physiology;
Trans-Activation (Genetics);
Transcription Factors/genetics/*metabolism
- From:Experimental & Molecular Medicine
2005;37(4):261-268
- CountryRepublic of Korea
- Language:English
-
Abstract:
Mouse embryonic stem (mES) cells are capable of undergoing chondrogenesis in vitro. To enhance this process, the human SOX9 (hSOX9) cDNA was delivered into mES cells and the clones overexpressing hSOX9 (denoted as mES-hSOX9 cells) were verified by Western blot analysis. The transcripts of collagen IIA (a juvenile form), aggrecan and Pax1 were expressed in mES-hSOX9 cells grown on feeder layers, suggesting the immediate effect of exogenous SOX9 on chondrogenesis. However, SOX9 overexpression did not affect the cell cycle distribution in undifferentiated mES cells. Upon differentiation, collagen IIB (an adult form) was detected in day 3 immature embryoid bodies. In addition, the overexpression of exogenous SOX9 significantly induced transcriptional activity driven by SOX9 binding site. Taken together, we for the first time demonstrated that constitutive overexpression of exogenous SOX9 in undifferentiated mES cells might have dual potentials to induce both chondrogenic commitment and growth capacity in the undifferentiated status.
