Abstract
The regulation of cell locomotion is a fundamental determinant of tissue architecture. Even in solid tissues of adult organisms cells often retain an intrinsic locomotor capacity which is activated during wound healing or tumor metastasis. In this study we have examined the role of cell locomotion in an in vitro model of thyroid epithelial pattern generation. Primary cultures of adult porcine thyroid cells reorganize to form follicles within three-dimensional cell aggregates when stimulated by thyrotropin (thyroid-stimulating hormone, TSH). Removal of TSH from the culture medium caused established follicles to reorganize into a confluent, two-dimensional epithelioid monolayer. The earliest observed change was the appearance of spreading cells at the peripheries of aggregates. These cells displayed broad lamellipodia whose formation was associated with the redistribution of microfilaments and microtubules and the accumulation of myosin. Spreading cells could migrate into, and fill, artificial wounds several millimeters wide without evidence of cell proliferation, indicating that cells became locomotile as they spread from follicles to form monolayer. Both spreading and migration were inhibited by cytochalasin B. In contrast, cells spread in the presence of colchine, but failed to migrate subsequently. Thyroid cell locomotility from follicles was inhibited by TSH, a cAMP analog, and a cell-free membrane fraction. However, migration from established monolayer cultures was not affected by these regulatory agents. This indicated that cell spreading was an important regulatory locus in thyroid cell patterning. We conclude that the tonic inhibition of thyroid cell locomotility contributes to the maintenance of follicular architecture in vitro. TSH and cell-cell contact may inhibit locomotion by preventing follicular cells from spreading, the earliest step in the morphogenetic conversion of follicles to monolayer.
Published Version
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