Azuma M, Tamatani T, Fukui K, Yuki T, Motegi K, Sato M
Second Department of Oral and Maxillofacial Surgery, Tokushima University School of Dentistry, Japan.
Arch Oral Biol. 1996 May;41(5):413-24. doi: 10.1016/0003-9969(96)00003-9.
To understand the specific cell type responsible for the synthesis of basement membrane components of the salivary gland, the effects of transforming growth factor (TGF)-beta 1 on morphological change, cellular proliferation and collagen synthesis were examined in these immortalized duct and myoepithelial cell clones, and the expression forms of their TGF-beta receptors analysed. When TGF-beta 1 was added to the cell clones in vitro, it induced a morphological alteration, with flattening in myoepithelial but not in duct cells. Although the growth of Mv1Lu mink lung epithelial cells was almost completely inhibited by TGF-beta 1, the duct and myoepithelial cells were partially resistant to such inhibition. By immunoblot analysis of immunoprecipitates, p53 was found bound to the simian virus-40 large T antigen, suggesting a functional loss of p53 in regulation of cell-cycle arrest. In the cloned myoepithelial cells but not the duct cells, TGF-beta 1 stimulated the production of type IV collagen. To attempt to understand the distinct responsiveness of cell clones to TGF-beta 1, the expression forms of TGF-beta receptors were examined by affinity cross-linking. Although the intensities of the cross-linked bands of the TGF-beta type II and type III receptors, particularly the type II, were weaker in the duct than the myoepithelial cell clones, the expression of the type II receptor mRNA was consistently detected in both clones. Accordingly, the reduction of TGF-beta 1 binding may have occurred at the post-transcriptional level. These findings imply that the cloned myoepithelial cells but not the cloned duct cells produce type IV collagen in response to TGF-beta 1 through the receptor-mediated signal transduction pathway, which is presumably disrupted in the cloned duct cells.
为了解负责唾液腺基底膜成分合成的特定细胞类型，我们检测了转化生长因子（TGF）-β1对这些永生化导管和肌上皮细胞克隆的形态变化、细胞增殖及胶原蛋白合成的影响，并分析了其TGF-β受体的表达形式。当在体外将TGF-β1添加到细胞克隆中时，它诱导了形态改变，肌上皮细胞出现扁平状，而导管细胞未出现。尽管TGF-β1几乎完全抑制了Mv1Lu貂肺上皮细胞的生长，但导管和肌上皮细胞对此种抑制具有部分抗性。通过对免疫沉淀物的免疫印迹分析，发现p53与猿猴病毒40大T抗原结合，这表明p53在调节细胞周期停滞方面功能丧失。在克隆的肌上皮细胞而非导管细胞中，TGF-β1刺激了IV型胶原蛋白的产生。为试图理解细胞克隆对TGF-β1的不同反应性，通过亲和交联检测了TGF-β受体的表达形式。尽管导管细胞克隆中TGF-β II型和III型受体的交联带强度，特别是II型，比肌上皮细胞克隆中的弱，但在两个克隆中均持续检测到II型受体mRNA的表达。因此，TGF-β1结合的减少可能发生在转录后水平。这些发现表明，克隆的肌上皮细胞而非克隆的导管细胞通过受体介导的信号转导途径对TGF-β1产生反应并产生IV型胶原蛋白，而克隆的导管细胞中该途径可能被破坏。
