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ATP Potentiates Insitol‐1,4,5‐triphosphate‐induced Calcium Release in Permeabilized Parotid and Pancreatic Acini
Author(s) -
Park Hyungseo,
Betzenhauser Matthew J.,
Won JongHak,
Wagner Larry E.,
Knowlton Lyndee M.,
Yule David I.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1181.2
Subject(s) - chemistry , intracellular , calcium , calcium in biology , medicine , endocrinology , microbiology and biotechnology , biology , biochemistry , organic chemistry
A pivotal event underlying exocytosis from exocrine cells is Ca 2+ mobilization from intracellular stores initiated by Insitol‐1,4,5‐triphosphate (InsP 3 ) binding to InsP 3 receptors (InsP 3 R). InsP 3 R gating is regulated by a diverse array of regulatory inputs. We aimed to investigate the effects of ATP on InsP 3 ‐induced Ca 2+ release in permeabilized parotid and pancreatic acini. ATP dependency is known to differ between InsP 3 R subtypes. Type II InsP 3 R is predominantly present in parotid gland, and both Type II and III InsP 3 R are expressed in pancreas. Following the SERCA driven filling of Ca 2+ stores, 0.1 μM to 10 μM InsP 3 was infused with or without ATP in β‐escin permeabilized acini. InsP 3 increased the Ca 2+ release rate in a concentration‐dependent manner in both parotid and pancreatic acini. ATP (5 mM) significantly enhanced Ca 2+ release at sub‐maximal [InsP 3 ]. Next, the ATP dependency of the InsP 3 ‐induced Ca 2+ release was tested. ATP dose‐dependently potentiated the 0.3 μM InsP 3 ‐induced Ca 2+ release rate in both parotid and pancreatic acini. However, the ATP concentration dependency was shifted to the left in parotid acini. These results provide evidence that ATP can enhance InsP 3 ‐induced Ca 2+ release in both parotid and pancreatic acini and that the complement of InsP 3 R in parotid acini is more sensitive to this form of regulation.