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通过调节细胞与基质之间的相互作用,在I型胶原上生长以及用12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯处理后,培养的上皮FL细胞中的细胞间接触和肌动蛋白丝的组织会发生改变。

Intercellular contacts and the organization of actin filaments in cultured epithelial FL cells are altered by growth on type I collagen and treatment with 12-O-tetradecanoylphorbol-13-acetate through the modulation of interactions between cells and the substratum.

作者信息

Shiba Y, Sastrodihardjo S, Sasaki Y, Kanno Y

机构信息

Department of Oral Physiology, Hiroshima University School of Dentistry, Japan.

出版信息

Cell Struct Funct. 1987 Dec;12(6):549-58. doi: 10.1247/csf.12.549.

DOI:10.1247/csf.12.549
PMID:3435916
Abstract

We have investigated the effects of various types of collagen and a tumor-promoting phorbol ester on intercellular contacts and the organization of actin in human amnion epithelial FL cells and mouse fibroblast 3T3-A31 cells. Our purpose was to investigate how modulation of interactions between cells and the substratum leads to alterations in intercellular contacts and organization of actin filaments. When cells were cultured on dishes coated with a solution containing type I collagen, but not type IV, changes were induced in the morphology of FL cells and their intercellular contacts. Type I collagen also caused changes in the organization of their actin filaments, although no such effects were observed with 3T3-A31 cells. In contrast, 12-O-tetradecanoylphorbol-13-acetate (TPA) caused morphological changes, dissociation of groups of cells, and reorganization of actin filaments in cultures of FL and 3T3-A31 cells. It also disrupted the sites of adhesion of FL cells to the substratum. Both type I collagen and TPA rapidly induced spreading of FL cells in the absence of serum. However, cis-hydroxyproline, known to inhibit secretion of collagen, did not suppress the TPA-induced dissociation of groups of FL cells. These results suggest that the interactions with type I collagen of epithelial FL cells, but not of fibroblastic 3T3-A31 cells, tend to disorganize cellular morphology, intercellular contacts, and actin filaments in ways similar to, but not directly related to, the effects of TPA.

摘要

我们研究了各种类型的胶原蛋白和一种促肿瘤佛波酯对人羊膜上皮FL细胞和小鼠成纤维细胞3T3 - A31细胞间接触及肌动蛋白组织的影响。我们的目的是研究细胞与基质之间相互作用的调节如何导致细胞间接触和肌动蛋白丝组织的改变。当细胞在涂有含I型胶原蛋白溶液(而非IV型胶原蛋白溶液)的培养皿上培养时,FL细胞的形态及其细胞间接触会发生变化。I型胶原蛋白还会引起其肌动蛋白丝组织的变化,尽管在3T3 - A31细胞中未观察到此类影响。相比之下,12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯(TPA)会导致FL细胞和3T3 - A31细胞培养物中的形态变化、细胞群体解离以及肌动蛋白丝的重新组织。它还破坏了FL细胞与基质的粘附位点。I型胶原蛋白和TPA在无血清的情况下均能迅速诱导FL细胞铺展。然而,已知可抑制胶原蛋白分泌的顺式羟脯氨酸并未抑制TPA诱导的FL细胞群体解离。这些结果表明,上皮FL细胞与I型胶原蛋白的相互作用,而非成纤维细胞3T3 - A31细胞与I型胶原蛋白的相互作用,倾向于以类似于但并非直接相关于TPA作用的方式破坏细胞形态、细胞间接触和肌动蛋白丝。

相似文献

1
Intercellular contacts and the organization of actin filaments in cultured epithelial FL cells are altered by growth on type I collagen and treatment with 12-O-tetradecanoylphorbol-13-acetate through the modulation of interactions between cells and the substratum.通过调节细胞与基质之间的相互作用,在I型胶原上生长以及用12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯处理后,培养的上皮FL细胞中的细胞间接触和肌动蛋白丝的组织会发生改变。
Cell Struct Funct. 1987 Dec;12(6):549-58. doi: 10.1247/csf.12.549.
2
12-O-tetradecanoylphorbol-13-acetate disrupts actin filaments and focal contacts and enhances binding of fibronectin-coated latex beads to 3T3-L1 cells.12-O-十四烷酰佛波醇-13-乙酸酯破坏肌动蛋白丝和黏着斑,并增强纤连蛋白包被的乳胶珠与3T3-L1细胞的结合。
Exp Cell Res. 1988 Oct;178(2):233-41. doi: 10.1016/0014-4827(88)90394-1.
3
Suppression by herbimycin A of 12-O-tetradecanoylphorbol-13-acetate-induced dissociation of cells and morphological changes in cultured FL and MDCK cells.赫伯霉素A对12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯诱导的培养FL和MDCK细胞解离及形态变化的抑制作用。
Jpn J Cancer Res. 1987 Nov;78(11):1216-23.
4
Possible involvement of reorganization of actin filaments, induced by tumor-promoting phorbol esters, in changes in colony shape and enhancement of proliferation of cultured epithelial cells.促癌佛波酯诱导的肌动蛋白丝重组可能参与培养的上皮细胞集落形状变化和增殖增强过程。
J Cell Physiol. 1987 Jul;132(1):49-56. doi: 10.1002/jcp.1041320107.
5
A tumor promoter induces rapid and coordinated reorganization of actin and vinculin in cultured cells.肿瘤启动子可诱导培养细胞中肌动蛋白和纽蛋白快速且协调的重组。
J Cell Biol. 1984 Sep;99(3):1045-59. doi: 10.1083/jcb.99.3.1045.
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Tumor promoter-induced disruption of junctional complexes in cultured epithelial cells is followed by the inhibition of cytokeratin and desmoplakin synthesis.肿瘤启动子诱导培养的上皮细胞中连接复合体的破坏,随后细胞角蛋白和桥粒斑蛋白的合成受到抑制。
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7
[Changes in the form and cytoskeleton of cultured fibroblasts as affected by 12-tetradecanoylphorbol-13-acetate].[十四烷酰佛波醇-13-乙酸酯对培养成纤维细胞形态和细胞骨架的影响]
Tsitologiia. 1987 Oct;29(10):1138-43.
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Tumor promoter and fibronectin induce actin stress fibers and focal adhesion sites in spreading human erythroleukemia (HEL) cells.肿瘤启动子和纤连蛋白可诱导正在铺展的人红白血病(HEL)细胞中形成肌动蛋白应激纤维和粘着斑。
Eur J Cell Biol. 1987 Oct;44(2):238-46.
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Phorbol ester-induced scattering of HT-29 human intestinal cancer cells is associated with down-modulation of E-cadherin.佛波酯诱导的HT-29人肠癌细胞散射与E-钙黏蛋白的下调有关。
J Cell Sci. 1993 Oct;106 ( Pt 2):513-21. doi: 10.1242/jcs.106.2.513.
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Tumor promoter-induced changes in the permeability of epithelial cell tight junctions.肿瘤启动子诱导上皮细胞紧密连接通透性的变化。
Cell. 1981 Jan;23(1):95-103. doi: 10.1016/0092-8674(81)90274-9.

引用本文的文献

1
Herbimycin A suppresses the reduction of gap-junctional intercellular communication induced by tumor-promoting phorbol ester in 3T3-L1 cells.除莠霉素A可抑制促肿瘤佛波酯诱导的3T3-L1细胞间隙连接细胞间通讯的减少。
Jpn J Cancer Res. 1989 Sep;80(9):855-60. doi: 10.1111/j.1349-7006.1989.tb01726.x.
2
Phorbol-ester-mediated expression of the collagen type I pro-alpha 2 gene in mouse 3T3-L1 cells and its absence in a phorbol 12-myristate 13-acetate-non-responsive variant.
Biochem J. 1991 Sep 1;278 ( Pt 2)(Pt 2):369-73. doi: 10.1042/bj2780369.