Peroxisome Proliferator-Activated Receptor gammaActivation Promotes Adipogenesis in Human Mesenchymal Stem Cells.
- Author:
Eun Jung KIM
1
;
Su Hyang KIM
;
Yun Hee KIM
;
Sung Jae KIM
;
Soo Bong HAHN
;
Jin Woo LEE
Author Information
1. Brain Korea 21 project for medical science, Yonsei University, Korea.
- Publication Type:Original Article
- Keywords:
Mesenchymal stem cell;
Adipocyte;
Peroxisome proliferator-activated receptor gamma;
Troglitazone;
Mitogen activated protein kinase
- MeSH:
Adipocytes;
Adipogenesis*;
Blotting, Western;
Bone Marrow;
Flow Cytometry;
Humans*;
Mesenchymal Stromal Cells*;
Peroxisome Proliferator-Activated Receptors;
Peroxisomes*;
Phosphorylation;
PPAR gamma;
RNA, Messenger
- From:Journal of Korean Orthopaedic Research Society
2003;6(1):127-134
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: In this study, we determined that the troglitazones could induce uniform adipogenesis of human mesenchymal stem cells (MSCs) within a short time in a dose- and a time-dependent manners. MATERIALS AND METHODS: Human MSCs were isolated from bone marrow and cultured in basal or adipogenic medium in the presence of 0~50 micrometer troglitazone for 5 days. Then we performed flow cytometry, RT-PCR and western blot analysis. RESULTS: In FACS assay, troglitazone induced adipocyte differentiation in a dose-dependent manner. At concentration of 25 micrometer troglitazone in adipogenic medium, over 50% of the cells differentiated into adipocytes at day 5. This was accompanied by increased mRNA levels for the adipocyte gene markers (LPL, aP2 and PPAR gamma) in RT-PCR. In western blot analysis, we found that ERK phosphorylation was inhibited in the early stage of adipogenesis. CONCLUSION: Through the addition of troglitazone as a PPAR gamma agonist, we could get the uniform adipogenic differentiation within a short time. Thus, troglitazone directly regulates differentiation of human MSCs into adipocytes; induced PPAR gamma expression may play a key regulatory role in this process. And we suggest a role for ERK as a regulatory switch for these differentiation pathways.
