Histamine inhibits ATP-induced [Ca2+](i) rise through the activation of protein kinase a in HL-60 cells
SCIE
SCOPUS
- Title
- Histamine inhibits ATP-induced [Ca2+](i) rise through the activation of protein kinase a in HL-60 cells
- Authors
- Song, SK; Suh, BC; Lee, HS; Kim, KT
- Date Issued
- 1997-03-19
- Publisher
- ELSEVIER SCIENCE BV
- Abstract
- We investigated the cross-talk between the histamine and ATP receptors in HL-60 human promyelocytes. While both histamine and extracellular ATP increase intracellular Ca2+ concentration ([Ca2+](i)), we found that histamine treatment causes a decrease in the subsequent ATP-induced Ca2+ release from intracellular stores and Ca2+ influx from extracellular space. In addition, histamine also inhibited the subsequent ATP-induced inositol 1,4,5-trisphosphate (IP3) generation in a manner comparable to the Ca2+ release. However, histamine did not inhibit thapsigargin-induced Ca2+ release and influx, thus indicating that histamine does not directly inhibit the Ca2+ release-activated channel (CRAC). Ca2+ elevation induced by 2'- and 3'-O-(4-benzoylbenzoyl) ATP (BzATP), which does not produce IP3, was also inhibited by treatment with histamine, suggesting the presence of ATP-gated channels that are regulated by histamine. Treatment with dibutyryl cAMP or 8-bromo-cAMP inhibited the subsequent ATP-induced response similar to histamine. Moreover, the incubation of cells with N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H89), a protein kinase A inhibitor, abolished histamine's inhibitory effect on the ATP-induced [Ca2+](i) rise and IP3 formation. These results suggest that histamine inhibits both ATP-induced IP3 production and ATP-activated channel opening, through protein kinase A activation. (C) 1997 Elsevier Science B.V.
- Keywords
- histamine; ATP, extracellular; [Ca2+](i); HL-60 cell; INCREASES CYTOSOLIC CA2+; HUMAN-NEUTROPHILS; PHOSPHOLIPASE-C; CYCLIC-AMP; PURINERGIC RECEPTORS; EXTRACELLULAR ATP; HL60 CELLS; CATION CHANNELS; DIBUTYRYL-CAMP; CALCIUM-ENTRY
- URI
- https://oasis.postech.ac.kr/handle/2014.oak/21355
- DOI
- 10.1016/S0014-2999(96)00998-3
- ISSN
- 0014-2999
- Article Type
- Article
- Citation
- EUROPEAN JOURNAL OF PHARMACOLOGY, vol. 322, no. 2-3, page. 265 - 273, 1997-03-19
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