Spreading of human neutrophils is immediately preceded by a large increase in cytoplasmic free calcium. Academic Article uri icon

Overview

abstract

  • When human polymorphonuclear leukocytes (PMN) are placed on various surfaces, they attach and spread rapidly, increasing their diameter severalfold. The spreading is associated with extensive changes in the cytoskeleton. Since many cytoskeletal events are regulated by Ca2+, we measured the cytosolic free calcium concentration ([Ca2+]i) in individual human PMN as they spread. [Ca2+]i was measured in single cells by microspectrofluorometry using the fluorescent Ca2+-sensitive dye fura-2. Immediately before spreading, PMN exhibit a rapid increase in [Ca2+]i, from 69 +/- 51 nM to 547 +/- 190 nM (mean +/- SD, n = 12). [Ca2+]i returns to near resting levels during the next minute, as the cells spread. Neither the spreading nor the [Ca2+]i spike is blocked by removal of extracellular calcium, by verapamil, by calmodulin antagonists, or by mitochondrial or microtubule poisons. Spreading, but not the [Ca2+]i increase, is blocked by the microfilament inhibitor cytochalasin B. Both spreading and the [Ca2+]i spike are blocked by ATP depletion and reversibly blocked by placing the cells in medium containing hypertonic sucrose or sodium chloride. These data strongly suggest that an increase in [Ca2+]i, derived from nonmitochondrial intracellular pools, plays an important role in the microfilament-mediated process of PMN spreading.

publication date

  • May 1, 1986

Research

keywords

  • Calcium
  • Neutrophils

Identity

PubMed Central ID

  • PMC323418

Scopus Document Identifier

  • 0022517083

Digital Object Identifier (DOI)

  • 10.1073/pnas.83.9.2919

PubMed ID

  • 3458251

Additional Document Info

volume

  • 83

issue

  • 9