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The role of STAT5 in osteogenesis of human bone-marrow mesenchymal stromal cells

Other Titles
 골수유래 중간엽 줄기세포의 골분화기간 동안에 STAT5A와 STAT5B의 역할 기능 분석 
Authors
 황지숙 
Issue Date
2013
Description
Dept. of Medical Science/석사
Abstract
Human bone-marrow mesenchymal stromal cells (MSCs) can differentiate into a variety of cell types such as adipocyte, chondrocyte, myoblast, and osteoblast, depending on induction conditions. The each process of differentiation is carried out by interaction of various proteins and hormones. The feasibility of therapeutic applications of MSCs has been raised based on these potential differentiation characteristics, however, the precise mechanism of differentiation has not yet been determined. As a possible regulator of MSCs differentiation, STAT proteins have been reported. STAT is a family of proteins consisted of 7 different types. They form either a homodimer or a heterodimer, and are phosphorylated by receptors for various growth factors and cytokines. Phosphorylation of STAT induces translocation of STAT to nuclei, then, STAT regulates the expression of target genes. In particular, STAT5 has been reported to accelerate the differentiation of MSCs to adipocytes. However, there relationship between STAT and differentiation of MSCs into osteoblast has hardly been studied. In this study, a series of studies have been carried out to determine the mechanism how STAT5A affects the human bone-marrow MSCs differentiation into osteoblast. When MSCs were induced to differentiate into osteoblast, the expression of STAT5A and STAT5B proteins were increased compared to the control cells. Knocking-down the expression of STAT5A with specific siRNAs promoted the differentiating of MSCs into osteoblast. Expressions of Runx2 and DLX5 proteins and mRNAs, marker genes for osteoblast, were confirmed to be increased in MSCs transfected with STAT5A siRNAs. In contrast, over-expression of STAT5A during the differentiating process of MSCs into osteoblast, decreased Runx2 and DLX5 at protein and mRNA levels. The transcriptional activity of the DLX5 promoter was decreased by over-expression of STAT5A and increased by knocking-down of STAT5A with siRNAs. In summary, these data suggest that the induction of MSC differentiation into osteoblast is mediated by DLX5 which is regulated by STAT5A as a pivotal transcription factor in osteogenesis.
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/134544
Appears in Collections:
2. Thesis / Dissertation (학위논문) > 1. College of Medicine (의과대학) > Master's Degree (석사)
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