Wound-induced calcium waves in alveolar type II cells

Abstract

Alveolar type II epithelial (ATII) cells repopulate the alveolus after acute lung injury. We hypothesized that injury would initiate signals in nearby survivors. When rat ATII monolayers were wounded, elevations in intracellular free Ca2+ concentration ([Ca2+]i) began at the edge of the wound and propagated outward as a wave for at least 300 μm. The [Ca2+]iwave was due to both influx of extracellular Ca2+ and release of intracellular Ca2+ stores. Reducing Ca2+ influx with brief treatments of ethylene glycol-bis(β-aminoethyl ether)- N, N, N′, N′-tetraacetic acid or Gd3+ reduced both the amplitude and the apparent speed. Draining intracellular Ca2+ stores by pretreatment with cyclopiazonic acid eliminated the [Ca2+]iwave. Therefore, the [Ca2+]iwave depended critically on intracellular Ca2+ stores. [Ca2+]ielevations propagated over a break in the monolayer, suggesting that extracellular pathways were involved. Furthermore, extracellular factors from injured cells elevated [Ca2+]iin uninjured cultures. We conclude that wounding produces a [Ca2+]iwave in surviving cells and part of this response is mediated by soluble factors released into the extracellular space during injury.

Multiple rows of cells behind an epithelial wound edge extend cryptic lamellipodia to collectively drive cell-sheet movement

“…Interestingly, it is known that cell-to-cell gap-junctionindependent cytosolic Ca 2+ waves are initiated by wounding in corneal epithelial cells, and extracellular ATP or UTP appear to mediate propagation of these waves (Klepeis et al, 2001). Similar results were obtained following wounding of alveolar epithelial cells (Hinman et al, 1997;Isakson et al, 2001). Furthermore, in MDCK cell monolayers, exogenously supplied ADP, ATP and UTP can accelerate wound closure (Kartha and Toback, 1992;Sponsel et al, 1995).…”

Identification of an AHNAK Binding Motif Specific for the Annexin2/S100A10 Tetramer

“…On the onehand,becauseA2tinteractionwiththemembraneiscalcium-dependent and because both H 2 O 2 treatment (45) and cellular wounding (46) can induce a rapid increase of intracellular calcium, one can speculate that the observed membrane localization of A2t is caused by transient calcium increase. On the other hand, oxidization treatment as well as wounding (47) may induce alteration of some membrane lipids such as peroxidation (48) that would promote binding of A2t.…”

Infiltration anesthetic lidocaine inhibits cancer cell invasion by modulating ectodomain shedding of heparin‐binding epidermal growth factor‐like growth factor (HB‐EGF)

“…It has been reported that wound stimulation increases intracellular calcium ([Ca 2þ ]i) in cells at the wounded edge (Hinman et al, 1997;Tran et al, 1999) and that Ca 2þ influx into the cytoplasm activates a membraneassociated metalloproteinase to process proHB-EGF by a pathway that does not require PKC (Dethlefsen et al, 1998). Ca 2þ ionophore increases [Ca 2þ ]i and lidocaine has been reported to attenuate the [Ca 2þ ]i oscillations in cardiomyocyte (McCaslin and Butterworth, 2000).…”