Hydra cell aggregate development is blocked by selective fragments of fibronectin and type IV collagen.
Hydra cell aggregate development is blocked by selective fragments of fibronectin and type IV collagen.
复制标题
水螅细胞聚集体的发育被纤连蛋白和 IV 型胶原蛋白的选择性片段阻断。
DOI：
10.1006/dbio.1994.1176
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发表时间：
1994
影响因子：
2.7
通讯作者：
SarrasJr,MP
中科院分区：
文献类型：
--
作者：
Zhang,X;Hudson,BG;SarrasJr,MP
水螅是一种简化的后生动物，其体壁由上皮双分子层和称为中胶层的细胞外基质组成。水螅已被证明具有许多在高等无脊椎动物和脊椎动物基质中看到的成分，包括纤维连接蛋白、IV型胶原蛋白、层粘连蛋白和硫酸肝素蛋白多糖。基于先前的研究表明细胞外基质成分对水螅发育至关重要，本研究旨在确定完整纤维连接蛋白及其各种功能域在水螅细胞聚集体发育中的作用。水螅细胞聚集包括由分离的水螅细胞形成的小球形成的完整的水螅。在这个发育过程中，细胞分离成上皮双分子层，然后在形态发生之前沉积新的细胞外基质。本研究结果表明，完整的纤维连接蛋白及其30kda明胶结合域是水螅细胞聚集发育的有效阻断剂。30 kda片段的明胶结合能力在还原后是最小的，在目前的研究中，该片段的还原和烷基化导致其阻止水螅细胞聚集发育的能力丧失。由于这些发现以及胶原与30kda明胶结合结构域相互作用的可能性，研究人员还对各种IV型胶原结构域进行了研究。这些研究表明，IV型胶原蛋白的NC1和7s结构域也是水螅细胞聚集发育的有效阻断剂。当使用纤维连接蛋白或IV型胶原蛋白抗体时，这些结果也被模拟。水螅细胞聚集体被阻断后，中胶层结构发生改变，细胞增殖受到抑制，细胞分化模式发生改变。这些结果表明，阻滞可能是由于中胶结构的改变，并伴随对细胞行为的影响。由此得出结论：(1)纤维连接蛋白和IV型胶原蛋白在水螅细胞聚集发育的早期阶段，即中胶层最初形成的阶段是至关重要的；(2)这些细胞外基质成分的片段对聚集发育的干扰导致水螅细胞分裂、细胞分化和形态发生的改变。
The Chidarian,Hydra, is a simplified metazoan whose body wall is composed of an epithelial bilayer with an intervening extracellular matrix termed the mesoglea. Hydra messoglea has been shown to have a number of components seen in higher invertebrate and vertebrate matrices, including fibronectin, type IV collagen, laminin, and heparan sulfate proteoglycan. Based on previous studies which indicated that extracellular matrix components are critical to hydra development, the current study was designed to determine the role of intact fibronectin and its various functional domains during development of hydra cell aggregates. Hydra cell aggregation involves the complete morphogenesis of adult hydra from pellets of dissociated hydra cells. During this development process, cells segregate into an epithelial bilayer and then deposit a new extracellular matrix prior to continuation of morphogenesis. Results from this study demonstrate that intact fibronectin and its 30-kDa gelatin binding domain are effective blockers of hydra cell aggregate development. The gelatin binding capacity of the 30-kDa fragment is lest upon reduction and in the present studies reduction and alkylation of this fragment resulted in a loss in its ability to block hydra cell aggregate development. Because of these findings and the potential for collagen interaction with the 30-kDa gelatin binding domain, studies were also performed with various type IV collagen domains. These studies indicated that both the NC1 and 7 S domains of type IV collagen were also effective blockers of hydra cell aggregate development. These results were mimicked when antibodies to fibronectin or type IV collagen were used. Structural changes in mesoglea, inhibition of cell proliferation, and changes in cell differentiation patterns accompanied the blockage of hydra cell aggregates. These results indicate that blockage may be due to alterations in mesoglea structure with accompanying affects on cell behavior. It is concluded that (i) fibronectin and type IV collagen are critical to the early stages of hydra cell aggregate development when the mesoglea is initially formed and that (ii) perturbation of aggregate development by fragments of these extracellular matrix components results in alterations in hydra cell division, cell differentiation, and morphogenesis.