During the high speed playback of this time-lapse sequence, the field of view is evocative of a congested intersection during rush hour traffic. All of the CRE BAG 2 cells seem to be trying to get somewhere else, but as more and more cells appear it becomes increasingly difficult for them to travel far without bumping into another cell. As the scene unfolds, it soon becomes evident that, unlike epithelial cells, fibroblasts generally demonstrate very little contact inhibition of migration. Similar to impatient motorists, the CRE BAG 2 cells seem to be unwilling to wait until traffic clears before embarking on their chosen paths, frequently opting to forge their own microscopic overpasses by crawling over other fibroblasts that lie in their way.

Even in the body, fibroblasts are capable of significant motility. When injury occurs, the cells, which are resident in connective tissue, rapidly migrate to the site of the wound. In vivo fibroblast locomotion, however, is not necessarily analogous to the movements of the cells in culture. This is because in a culture dish, the fibroblasts adhere to the substratum, essentially confining their movements to two dimensions. The importance of the substratum to cultured cell motility is demonstrated by the flattening of daughter cells that occurs soon after they are produced by a parent cell. Without an adjacent solid surface, daughter fibroblast cells would not predictably assume the same form.

Cultured CRE BAG 2 cells move about their environment via cycles of lamellipodia extension and contraction. Lamellipodia formation is most dominant along the leading margins of the fibroblasts. As they are extended out across the culture medium, they form close points of contact with the substratum called focal adhesions. These junctions remain stationary as the cell harnesses the force of traction to pull itself over them. When the focal adhesions become too distal from the front edge of a cell, they are usually released in order that they do not hinder the cell’s advancement.