Spine · 2011
Isolation of mesenchymal stem cells from human ligamentum flavum: implicating etiology of ligamentum flavum hypertrophy.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Chen Yi-Te, Wei Jyh-Ding, Wang Jung-Pan, Lee Hsieh-Hsing, Chiang En-Rung, Lai Hung-Chang, Chen Ling-Lan, Lee Yi-Ting, Tsai Chih-Chien, Liu Chien-Lin, Hung Shih-Chieh
Аннотация
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.
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.
Предметные рубрики MeSH
ActinsAdipocytesBlotting, WesternCell DifferentiationCell ProliferationCells, CulturedChondrocytesCollagenGene ExpressionHistone Deacetylase InhibitorsHumansHydroxamic AcidsHypertrophyImmunohistochemistryLigamentum FlavumMesenchymal Stem CellsMuscle, SmoothOsteoblastsOsteopontinReverse Transcriptase Polymerase Chain ReactionTransforming Growth Factor beta1