INVIVO DEMONSTRATION OF CELL-TYPES IN BONE THAT HARBOR EPIDERMAL GROWTH-FACTOR RECEPTORS

INVIVO DEMONSTRATION OF CELL-TYPES IN BONE THAT HARBOR EPIDERMAL GROWTH-FACTOR RECEPTORS
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DOI:
10.1210/endo-123-2-841
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发表时间:
1988-08-01
期刊:
影响因子:
4.8
通讯作者:
BERGERON, JJM
BERGERON, JJM
中科院分区:
医学2区
文献类型:
--
作者:
MARTINEAUDOIZE, B;LAI, WH;BERGERON, JJM

文献摘要

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用放射自显影技术原位观察了[~(125)I]碘-表皮生长因子(EGF)与大鼠骨细胞的结合和内化。在富含内吞成分的细胞轮廓上观察到特定的结合部位,包括溶酶体样结构、粗面内质网丰富的细胞轮廓以及组织学上类似于未分化前体细胞的细胞轮廓。根据凝胶过滤和三氯乙酸的沉淀性标准,结合的[125I]碘-EGF大部分被认为是完整的。根据形态标准,结合[125I]碘-EGF的细胞轮廓中没有一种与完全形成的破骨细胞或成骨细胞相对应。内吞细胞位于侵袭的毛细血管与软骨横隔部和纵隔部之间的骨骺板内,在混合毛刺区的破骨细胞附近。靠近干骺端的骨干板软骨细胞陷窝内可见富含粗面内质网的细胞,干骺端的混合针之间可见低分化的细胞。在门牙周围的牙槽骨中也发现了类似的细胞类型。这些细胞可能是已建立的含有高浓度EGF受体的骨细胞系的来源,也可能是体液高钙血症的原因,以回应已报道的注射EGF或转化生长因子-α的作用。以及恶毒的影响。
The binding and internalization of [125I]iodo-epidermal growth factor (EGF) by bone cells of the rat was demonstrated in situ by quantitative radioautography. Specific binding sites were observed on a cell profile enriched in endocytic components, including lysosome-like structures, a rough endoplasmic reticulum-rich cell profile, and a cell profile that histologically resembles an undifferentiated precursor cell. By the criteria of gel filtration and precipitability by trichloroacetic acid, most of the bound [125I]iodo-EGF was considered intact. By morphological criteria none of the cell profiles that bound [125I]iodo-EGF corresponded to fully formed osteoclasts or osteoblasts. The endocytic cell was found in the epiphyseal plate between the invading capillary and the transverse and longitudinal cartilage septa as well as near osteoclasts in the zone of mixed spicules. The rough endoplasmic reticulum-rich cell was present in vacated chondrocyte lacunae of the epiphyseal plate close to the metaphysis, and the poorly differentiated cell was observed between the mixed spicules of the metaphysis. Similar cell types were also found in the alveolar bone surrounding the incisors. These cells may be the origin of established bone cell lines that harbor high concentrations of EGF receptors and may also be responsible for the humoral hypercalcemia in response to the reported actions of injected EGF or transforming growth factor-.alpha. as well as that of malignancy.