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Title: Functional properties of the type-3 InsP3 receptor in 16HBE14o- bronchial mucosal cells
Authors: Missiaen, Ludwig
Parys, Jan
Sienaert, Ilse
Maes, K
Kunzelmann, K
Takahashi, M
Tanzawa, K
De Smedt, Humbert #
Issue Date: May-1998
Series Title: Journal of Biological Chemistry vol:273 issue:15 pages:8983-6
Abstract: The type-3 inositol 1,4,5-trisphosphate (InsP3) receptor is the major isoform expressed in 16HBE14o- cells from bronchial mucosa, representing 93% at the mRNA level as determined by ratio reverse transcription-polymerase chain reaction and about 81% at the protein level as determined with isoform-specific antibodies (Sienaert, I., Huyghe, S., Parys, J. B., Malfait, M., Kunzelmann, K., De Smedt, H., Verleden, G. M., and Missiaen, L., Pflügers Arch. Eur. Y. Physiol., in press). The present 45Ca2+ efflux experiments indicate that these InsP3 receptors were 3 times less sensitive to InsP3 and 11 times less sensitive to ATP than those in A7r5 cells, where the type-1 InsP3 receptor is the main isoform. ATP did not increase the cooperativity of the InsP3-induced Ca2+ release in 16HBE14o- cells, in contrast to its effect in A7r5 cells. The sulfhydryl reagent thimerosal also did not stimulate InsP3-induced Ca2+ release in 16HBE14o- cells, again in contrast to its effect in A7r5 cells. Adenophostin A was more potent than InsP3 in stimulating the release in both cell types. The biphasic activation of the InsP3 receptor by cytosolic Ca2+ occurred in both cell types. We conclude that Ca2+ release mediated by the type-3 InsP3 receptor mainly differs from that mediated by the type-1 InsP3 receptor by its lack of stimulation by sulfhydryl oxidation and its lower ATP and InsP3 sensitivity. The predominant expression of the type-3 InsP3 receptor in the bronchial mucosa may be part of a mechanism coping with oxidative stress in that tissue.
URI: 
ISSN: 0021-9258
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Physiology Section (-)
Laboratory of Molecular and Cellular Signaling
# (joint) last author

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