Bodo M, Venti G, Baroni T, Bellucci C, Giammarioli M, Donti E, Paludetti G, Stabellini G, Carinci P
Istituto di Istologia ed Embriologia generale, Università di Ferrara, Italy.
Cell Mol Biol (Noisy-le-grand). 1995 Dec;41(8):1039-49.
A study was carried out to obtain a more detailed picture of the phenotypes of human otosclerotic and normal bone cells and to analyse the response of both populations to treatment with TGF beta 1. Total collagen synthesis was found to be decreased, but fibronectin secretion increased in otosclerotic with respect to normal cells. Although overall glycosaminoglycan (GAG) synthesis was lower in otosclerotic cells, the sulphated GAG to hyaluronic acid (HA) ratio was higher, in particular there was greater expression of chondroitin (CS) and dermatan sulphates (DS). TGF beta 1 induced a more marked increase in collagen and fibronectin release and greater production of sulphated GAGs as DS and heparan sulphate (HS) in the otosclerotic cells. The fact that the phenotype of the otosclerotic cells differed from that of the normal cells and could be modified by TGF beta 1 treatment, suggests that TGF beta 1 is implicated in the pathogenesis of otosclerosis.
开展了一项研究，以更详细地了解人类耳硬化症和正常骨细胞的表型，并分析这两类细胞群体对转化生长因子β1（TGF beta 1）治疗的反应。研究发现，与正常细胞相比，耳硬化症细胞的总胶原蛋白合成减少，但纤连蛋白分泌增加。虽然耳硬化症细胞中糖胺聚糖（GAG）的总体合成较低，但硫酸化GAG与透明质酸（HA）的比率较高，特别是硫酸软骨素（CS）和硫酸皮肤素（DS）的表达更高。TGF beta 1诱导耳硬化症细胞中胶原蛋白和纤连蛋白释放的增加更为显著，并且硫酸化GAG（如DS和硫酸乙酰肝素（HS））的产生更多。耳硬化症细胞的表型与正常细胞不同，并且可以通过TGF beta 1治疗进行改变，这一事实表明TGF beta 1与耳硬化症的发病机制有关。
