A regulated, coordinated movement of cytoplasm is essential for the function of phagocytes. In these cells, as in muscle cells, the power unit for movement consists of the contractile proteins, actin and myosin, which are concentrated in the region of the cell cortex. In the peripheral cytoplasm, actin fibres may be in a fluid state or they may form a gel network by association with a homodimeric, actin-binding protein. The reversible transformation of the cytoplasm from gel to sol is mediated by a regulatory protein called gelsolin, which when activated by micromolar concentrations of Ca2+, causes shortening of actin fibres, leading to disintegration of the gel network. This gel network reforms if the Ca2+ concentration falls below the threshold value for the activation of gelsolin. Ca2+, acting via gelsolin, is a second component in this system; it controls the order of events that start on the plasma membrane of the phagocyte in response to a stimulus, and are then maintained by an appropriate reaction of the contractile unit. It is to be expected that the elucidation of the molecular mechanisms that release and regulate the movement of cytoplasm in the cell will permit an understanding of factors that interfere with leukocyte function.
|Original language||English (US)|
|Number of pages||10|
|Journal||Journal of Clinical Chemistry and Clinical Biochemistry|
|State||Published - 1983|
ASJC Scopus subject areas
- Clinical Biochemistry