Isolation of mesenchymal stem cells from human ligamentum flavum: implicating etiology of ligamentum flavum hypertrophy
| Autor: | Yi Te Chen, Hsieh Hsing Lee, Ling Lan Chen, Hung Chang Lai, Shih-Chieh Hung, Jyh Ding Wei, Chien Lin Liu, Chih Chien Tsai, Yi Ting Lee, En Rung Chiang, Jung Pan Wang |
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| Rok vydání: | 2011 |
| Předmět: |
medicine.drug_class
Blotting Western Connective tissue Gene Expression Hydroxamic Acids Muscle hypertrophy Pathogenesis Transforming Growth Factor beta1 Chondrocytes Adipocytes Medicine Humans Orthopedics and Sports Medicine Cells Cultured Cell Proliferation Osteoblasts business.industry Cell growth Reverse Transcriptase Polymerase Chain Reaction Histone deacetylase inhibitor Mesenchymal stem cell Cell Differentiation Mesenchymal Stem Cells Muscle Smooth Hypertrophy Immunohistochemistry Actins Cell biology Histone Deacetylase Inhibitors Trichostatin A medicine.anatomical_structure Ligamentum Flavum Osteopontin Neurology (clinical) Bone marrow Collagen business medicine.drug |
| Zdroj: | Spine. 36(18) |
| ISSN: | 1528-1159 |
| Popis: | Study design To demonstrate the existence of mesenchymal stem cells (MSCs) in ligamentum flavum (LF) and their pathogenic role in LF hypertrophy. Objective To isolate and characterize LF-derived MSCs and their response to transforming growth factor-beta 1 (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 pathogenic role of TGF-β1 in spinal stenosis has been implicated. 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. MSCs have been isolated from a variety of adult tissues, except LF. Whether MSCs exist in LF and their response to TGF-β1 and TSA is not clear. 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 similar 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. Conclusion The current results demonstrated the isolation of MSCs from LF. The cellular response to TGF-β1 implied that these cells might 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. |
| Databáze: | OpenAIRE |
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