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Resealing of a disrupted plasma membrane in the micron-size range requires Ca(2+)-regulated exocytosis. When cells are wounded twice, the second membrane disruption reseals more quickly than the initial wound. This response is protein kinase C (PKC)-dependent and protein kinase A dependent in the early stages. In the long term (24 h), potentiation of membrane resealing in a wounded cell depends on gene expression mediated by a transcription factor, cyclic adenosine monophosphate response element binding protein(CREB), which is activated by a PKC-dependent and p38 mitogen-activated protein kinase-dependent pathway. In addition,a recent study demonstrated that wounding of Madin–Darby canine kidney (MDCK) cells potentiates membrane resealing in neighboring cells by activating CREB-dependent gene expression through nitric oxide (NO) signaling. The present study demonstrated that wounding of MDCK cells induces short-term potentiation of membrane resealing in neighboring cells in addition to a long-term response. Inhibition of purinergic signaling suppressed short-term potentiation of membrane resealing in neighboring cells, but not long-term potentiation. By contrast, inhibition of NO signaling did not suppress the short-term response in neighboring cells. These results suggest that cell membrane disruption stimulates at least two intercellular signaling pathways, NO and purinergic signaling, to potentiate cell membrane resealing in neighboring cells.

Short-term potentiation of membrane resealing in neighboring cells is mediated by purinergic signaling