Intercellular Propagation of Calcium Waves Mediated by Inositol Trisphosphate

Abstract

Two types of calcium (Ca2+) signaling-propagating intercellular Ca2+ waves of increasing intracellular Ca2+ concentration ([Ca2+]i) and nonpropagating oscillations in [Ca2+]i-co-exist in a variety of cell types. To investigate this difference in Ca2+ signaling, airway epithelial cells were loaded with heparin, an inositol 1,4,5-triphosphate (IP3) receptor antagonist, by pulsed, high-frequency electroporation. Heparin inhibited propagation of intercellular Ca2+ waves but not oscillations of [Ca2+]i. In heparin-free cells, Ca2+ waves propagated through cells displaying [Ca2+]i oscillations. Depletion of intracellular Ca2+ pools with the Ca2+-pump inhibitor thapsigargin also inhibited the propagation of Ca2+ waves. These studies demonstrate that the release of Ca2+ by IP3 is necessary for the propagation of intercellular Ca2+ waves and suggest that IP3 moves through gap junctions to communicate intercellular Ca2+ waves.

Synchronized calcium spiking resulting from spontaneous calcium action potentials in monolayers of NRK fibroblasts

“…In most cases, the underlying mechanism was unknown. In other cell types, intercellularly propagating Ca2+ waves have been reported [30,33,34] that probably result from the regenerative production of IP3 by the diffusion of Ca2+ and/or IP3 through gap junctions to neighbouring cells with concomitant Ca2+ release from intracellular stores [2].…”

Membrane Targeting and Coupling of NHE1-IntegrinαIIbβ3-NCX1 by Lipid Rafts following Integrin-Ligand Interactions Trigger Ca2+ Oscillations

“…As a general rule, calcium entry through voltage-gated channels in electrically excitable cells (3) or through agonist-receptor interactions in nonexcitable cells, such as epithelial cells, hepatocytes, or oocytes (4), is thought to initiate the CICR process (1,2). Typically, in nonexcitable cells, the binding of an agonist, such as a hormone, a growth factor, or an extracellular matrix, to the corresponding cell surface receptor initiates a series of reactions that end in the activation of phopholipase C (PLC) and the production of the secondary messenger inositol trisphosphate (IP 3 ) (1,2,4).…”

“…Typically, in nonexcitable cells, the binding of an agonist, such as a hormone, a growth factor, or an extracellular matrix, to the corresponding cell surface receptor initiates a series of reactions that end in the activation of phopholipase C (PLC) and the production of the secondary messenger inositol trisphosphate (IP 3 ) (1,2,4). IP 3 is thought to induce calcium release from the internal endoplasmic reticulum or mitochondria store, and governs the CICR mechanisms that modulate calcium oscillations (1,2,4). However, not all calcium oscillations found in nonexcitable cells are initiated by the PLC-IP 3 pathway (5).…”

Effects of dynamic compression on lentiviral transduction in an in vitro airway wall model

“…In actual bronchi, cilia sweep upward to remove debris from the lungs, but since our model was symmetric in the x and y directions (without strain) we did not expect an overall directionality. The effects of dynamic strain on ciliary motion were not considered in this work, although it has been previously shown that mechanical stimulation leads to intra-and intercellular Ca 2ϩ signaling that would increase ciliary beat frequency (5,56,66). Therefore, the increase in overall infection rate that we see is unlikely to be due to any changes in ciliary beat frequency or coordination.…”