Autocrine signaling through ATP release represents a novel mechanism for cell volume regulation.
-
- Y Wang
- Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
-
- R Roman
- Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
-
- S D Lidofsky
- Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
-
- J G Fitz
- Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.
抄録
<jats:p>Recovery of cell volume in response to osmotic stress is mediated in part by increases in the Cl- permeability of the plasma membrane. These studies evaluate the hypothesis that ATP release and autocrine stimulation of purinergic (P2) receptors couple increases in cell volume to opening of Cl- channels. In HTC rat hepatoma cells, swelling induced by hypotonic exposure increased membrane Cl- current density to 44.8 +/- 7.1 pA/pF at -80 mV. Both the rate of volume recovery and the increase in Cl- permeability were inhibited in the presence of the ATP hydrolase apyrase (3 units/ml) or by exposure to the P2 receptor blockers suramin and Reactive Blue 2 (10-100 microM). Cell swelling also stimulated release of ATP. Hypotonic exposure increased the concentration of ATP in the effluent of perfused cells by 170 +/- 36 nM in the presence of a nucleotidase inhibitor (P < 0.01). In whole-cell recordings with ATP as the charge carrier, cell swelling increased membrane current density approximately 30-fold to 16.5 +/- 10.4 pA/pF. These findings indicate that increases in cell volume lead to efflux of ATP through opening of a conductive pathway consistent with a channel, and that extracellular ATP is required for recovery from swelling. ATP may function as an autocrine factor that couples increases in cell volume to opening of Cl- channels through stimulation of P2 receptors.</jats:p>
収録刊行物
-
- Proceedings of the National Academy of Sciences
-
Proceedings of the National Academy of Sciences 93 (21), 12020-12025, 1996-10-15
Proceedings of the National Academy of Sciences
- Tweet
キーワード
詳細情報 詳細情報について
-
- CRID
- 1361699995610596096
-
- NII論文ID
- 30016219671
-
- ISSN
- 10916490
- 00278424
- http://id.crossref.org/issn/13460706
-
- データソース種別
-
- Crossref
- CiNii Articles