Isolation of mesenchymal stem cells from human ligamentum flavum: implicating etiology of spinal stenosis

碩士 === 國立陽明大學 === 臨床醫學研究所 === 98 === Study Design. To prove the existence of mesenchymal stem cells (MSCs) in ligamentum flavum (LF). Objective. To isolate and characterize LF-derived MSCs and their response to transforming growth factor-beta1 (TGF-β1) and trichostatin A (TSA), a histone deacetyla...

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Bibliographic Details
Main Authors: Yi-Te Chen, 陳怡德
Other Authors: Shih-Chieh Hung
Format: Others
Language:en_US
Published: 2010
Online Access:http://ndltd.ncl.edu.tw/handle/31185074405310499531
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Summary:碩士 === 國立陽明大學 === 臨床醫學研究所 === 98 === Study Design. To prove the existence of mesenchymal stem cells (MSCs) in ligamentum flavum (LF). Objective. To isolate and characterize LF-derived MSCs and their response to transforming growth factor-beta1 (TGF-β1) and trichostatin A (TSA), a histone deacetylase inhibitor (HDACi). Summary of Background Data. LF is a connective tissue, of which hypertrophic changes induce spinal stenosis. The pathogenetic role of TGF-β1 in spinal stenosis has been implicated. MSCs have been isolated from a variety of adult tissues, except LF. TSA has been shown to suppress TGF-β1-induced alpha-smooth muscle actin (α-SMA), type I and III collagen synthesis in a variety of cells. Methods. The MSCs from LF were isolated and cultured. Their phenotypic character, linage differentiation potential and response to TGF-β1 and TSA were analyzed. Results. LF-derived MSCs have the same profile of surface markers as bone marrow MSCs. They were demonstrated to have the potential to be differentiated into osteoblasts, adipocytes and chondrocytes. Administration of TGF-β1 stimulated cell proliferation, enhanced the gene expression of type I and III collagen, and increased the gene expression and protein level of α-SMA. TSA blocked the fibrogenic effects of TGF-β1. Conclusions. The current results demonstrated the isolation of MSCs from LF, which may serve as a potential source for tissue engineering. The cellular response to TGF-β1 implied these cells may play an important role in the pathogenesis of LF hypertrophy. TSA, which blocks the effects of TGF-β1, may be a potent therapeutic choice for inhibiting LF hypertrophy.