Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 25, Issue 1, Pages 91-102Publisher
KARGER
DOI: 10.1159/000272064
Keywords
Alveolar type II cells; NCI-H441 cells; 2-APB; Capsazepine; Ca2+; Endocytosis
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Funding
- DFG [D1402]
- FWF [P15743]
- European Union (Pulmo-Net)
- Boehringer Ingelheim
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Calcium as a second messenger influences many cellular and physiological processes. In lung, alveolar type II (ATII) cells sense mechanical stress and respond by Ca2+ dependent release of surfactant, which is essential for respiratory function. Nevertheless, Ca2+ signaling mechanisms in these cells-in particular Ca2+ entry pathways are still poorly understood. Herein, we investigated pharmacological properties of non-voltage-gated Ca2+ channel modulators in ATII and NCI-H441 cells and demonstrate that 2-Aminoethoxydiphenyl-borinate (2-APB) and capsazepine (CPZ) activate Ca2+ entry with pharmacologically distinguishable components. Surprisingly, 2-APB and CPZ activated clathrin dependent endocytosis in ATII and NCI-H441 cells, which was dependent on Ca2+ entry. The internalized material accumulated in non-acidic granules distinct from surfactant containing lamellar bodies (LB). LB exocytosis was not observed under these conditions. Our study demonstrates that 2-APB/CPZ induces Ca2+ entry which unlike ATP-or stretch-induced Ca2+ entry in ATII cells does not activate exocytosis but an opposing endocytotic mechanism. Copyright (C) 2010 S. Karger AG, Basel
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