Nanomedicine, Volume I: Basic Capabilities

© 1999 Robert A. Freitas Jr. All Rights Reserved.

Robert A. Freitas Jr., Nanomedicine, Volume I: Basic Capabilities, Landes Bioscience, Georgetown, TX, 1999 Amoeboid Locomotion

The most common cells exhibiting amoeboid locomotion3613 in the human body are white cells, having moved out of the blood into the tissues in the form of tissue microphages or macrophages. Fibroblasts and normally sessile germinal skin cells can move into damaged areas to assist in wound repair. Embryonic cells in the fetus such as neurons often migrate long distances to their final location by amoeboid movement, after which they become fixed in tissue as sessile cells. The 200-600 micron carnivorous Amoeba proteus also displays this form of locomotion and was the subject of the earliest studies, hence the name.

Amoeboid movement is associated with two properties -- cytoplasmic streaming, and the extension and retraction of pseudopods -- the motive effects of which could be simulated by medical nanorobots using metamorphic exterior surfaces (Section 5.3). As shown in Figure 9.26, the monopodial amoeboid cell progresses by establishing a series of attachment points or focal contacts with the surface it is traversing. Viewed from the side, the amoeba steps forward on new pseudopods that make adhesive contact with the surface, with the tail region and retracting pseudopods lifted clear of the surface.1464 The plasma membrane with its mucus coat is a relatively permanent structure that plays a passive role during locomotion,1465 rotating forward during locomotion something like a water balloon rolling across a tilted tabletop.

Inside the plasma membrane are two regions of cytoplasm with varying viscosity -- the actin microfilament-rich outer portion, called the ectoplasm or cell cortex, and the inner portion called the endoplasm. To move forward, the ectoplasm at the front end becomes thin, causing a pseudopodium to bulge forward; the ectoplasm at the tail end contracts, pushing endoplasm into the pseudopodium and extending it further.1466 Actin monomers in the pseudopods are gelated to actin polymers in the pseudopods, then solated back to monomers in the tail. (Gels depolymerize when Ca++ activates gelsolin protein, which severs actin; actin repolymerizes into gel when Ca++ concentration is reduced.) The surface for new pseudopod formation is unfolded from the sink of convoluted surface in retracted pseudopods and in the tail. In each pseudopod, the surface rolls forward over the stationary ectoplasmic tube on a lubricating layer of hyaloplasm dispersed from the hyaline cap.1380 Isolated amoebic cytoplasm, when injected with ATP, streams spontaneously at up to 160 microns/sec.1394

The formation of a focal contact between fibroblast and surface is a biphasic process in which the fast (~1 sec) initial phase of establishing small (~0.25 micron2) immature contacts at large separation distances is followed by a slower (~15 sec) phase of widening mature contacts with narrowing separation distances.1457 Leukocyte pseudopodia are ~1 micron in length with a typical extension velocity of ~0.08 microns/sec,846 so white cells and fibroblasts readily cytoambulate at ~0.05-0.1 micron/sec;359,1513 chemotactically-stimulated leukocytes can locomote at up to ~0.7 microns/sec.1516 An individual fibroblast has a towing strength of ~165 nN,1461 giving an implied low-load motive power demand of only ~0.02 pW (force x velocity). Measured motive force of a whole amoeba (~towing force) is 50-290 nN,1462,1469 or ~100 nN per 50-micron pseudopod; internal hydrostatic pressures have been estimated from 10-100 N/m2 1470,1471 up to ~105 N/m2.1453 Ambulatory velocity ranges from 1-50 microns/sec, but averages ~10 microns/sec.1394 A nanorobot using metamorphic pseudopods spaced ~1 micron apart and cycling its adhesive contacts at 10 KHz could achieve vnano ~ 1 cm/sec within a ~10 pW motive power budget (Section

Neutrophils walk from one site to another by forming and breaking integrin-mediated attachments to a matrix (Fig. 9.27). Integrin receptor surface density is ~2000/micron2 on neutrophils,1510 with each fibrinogen attachment having a detachment strength of ~2 pN.1508


Last updated on 21 February 2003