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首页> 美国卫生研究院文献>Annals of the Rheumatic Diseases >Transforming growth factor β1 and interleukin 4 induced α smooth muscle actin expression and myofibroblast-like differentiation in human synovial fibroblasts in vitro: modulation by basic fibroblast growth factor
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Transforming growth factor β1 and interleukin 4 induced α smooth muscle actin expression and myofibroblast-like differentiation in human synovial fibroblasts in vitro: modulation by basic fibroblast growth factor

机译：体外人滑膜成纤维细胞中转化生长因子β1和白介素4诱导的α平滑肌肌动蛋白表达及成肌纤维样分化：碱性成纤维细胞生长因子的调控

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OBJECTIVE—To discover if α smooth muscle actin expression and myofibroblastic differentiation are induced in synovial fibroblasts by cytokines found in the inflamed RA joint.
METHODS—Immunofluorescent microscopy and western blotting were used to examine different cultures of human synovial fibroblasts for expression of α actin in the presence of the cytokines transforming growth factor β (TGFβ1), interleukin 1α (IL1α), IL4, IL6, tumour necrosis factor α (TNFα), and basic fibroblast growth factor (FGF).
RESULTS—A small but significant population of cells (14.4 ± 12.9%) expressed α actin under standard culture conditions. Upon treatment with TGFβ1 there was a pronounced increase in the number of cells expressing α actin (68.1 ± 5.49%), accompanied by a change in morphology to a myofibroblast-like phenotype. Other cytokines found within the inflamed joint such as IL1, TNFα , IL6, and basic FGF failed to induce α actin expression. However, IL4, which is normally absent or only present at low concentrations in the RA joint had a similar effect to TGFβ1. It was also found that basic FGF inhibited the induction of α actin expression by TGFβ1 and IL4.
CONCLUSION—In the presence of TGFβ1 or IL4, fibroblasts derived from synovial tissue or synovial fluid are induced to differentiate into myofibroblast-like cells containing the α smooth muscle form of actin. This differentiation is inhibited by basic FGF. It is suggested that the balance between these particular cytokines may be important in the modulation of fibroblast behaviour, which could have significant effects on joint repair mechanisms and the generation of fibrous tissue within the rheumatoid joint.
机译：目的—探讨是否通过发炎的RA关节中发现的细胞因子在滑膜成纤维细胞中诱导α平滑肌肌动蛋白表达和肌成纤维细胞分化。细胞转化生长因子β（TGFβ1），白介素1α（IL1α），IL4，IL6，肿瘤坏死因子α（TNFα）和碱性成纤维细胞生长因子（FGF）存在下α肌动蛋白的表达。
结果—在标准培养条件下，少量但重要的细胞群（14.4±12.9％）表达α肌动蛋白。用TGFβ1处理后，表达α肌动蛋白的细胞数量显着增加（68.1±5.49％），并伴随着成肌纤维细胞样表型的形态改变。发炎的关节内发现的其他细胞因子如IL1，TNFα，IL6和碱性FGF无法诱导α肌动蛋白表达。但是，通常在RA关节中不存在或仅以低浓度存在的IL4具有与TGFβ1类似的作用。还发现碱性FGF抑制TGFβ1和IL4诱导α肌动蛋白表达。
结论—在存在TGFβ1或IL4的情况下，滑膜组织或滑液衍生的成纤维细胞被诱导分化为成肌纤维细胞样细胞。含有肌动蛋白的α平滑肌形式。这种分化被碱性FGF抑制。提示这些特定细胞因子之间的平衡可能对调节成纤维细胞的行为很重要，这可能对关节修复机制和类风湿关节内纤维组织的产生产生重要影响。

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