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DOE OSTI2018

Role of inositol 1,4,5-trisphosphate receptor type 1 in ATP-induced nuclear Ca2+ signal and hypertrophy in atrial myocytes

Highlights: • IP{sub 3} receptor type 1 (IP{sub 3}R1) are expressed in atrial cell perinucleus. • IP{sub 3}R1 mediates ATP-induced sustained nuclear Ca{sup 2+} increase in HL-1 atrial cells. • IP{sub 3}R1 contributes to higher sensitivity of nuclear release sites upon IP{sub 3} increase. • Larger Ca{sup 2+} content in perinuclear store of atrial cells involves IP{sub 3}R1. • IP{sub 3}R1 signaling may play a role in ATP-induced atrial cell hypertrophy. Inositol 1,4,5-trisphosphate receptor type 1 (IP{sub 3}R1) is expressed in atrial muscle, but not in ventricle, and they are abundant in the perinucleus. We investigated the role of IP{sub 3}R1 in the regulations of local Ca{sup 2+} signal and cell size in HL-1 atrial myocytes under stimulation by IP{sub 3}-generating chemical messenger, ATP. Assessment of nuclear and cytosolic Ca{sup 2+} signal using confocal Ca{sup 2+} imaging revealed that IP{sub 3} generation by ATP (1 mM) induced monophasic nuclear Ca{sup 2+} increase, followed by cytosolic Ca{sup 2+} oscillation. Genetic knock-down (KD) of IP{sub 3}R1 eliminated the monophasic nuclear Ca{sup 2+} signal and slowed the cytosolic Ca{sup 2+} oscillation upon ATP exposure. Prolonged application of ATP as well as other known hypertrophic agonists (endothelin-1 and phenylephrine) increased cell size in wild-type cells, but not in IP{sub 3}R1 KD cells. Our data indicate that IP{sub 3}R1 mediates sustained elevation in nuclear Ca{sup 2+} level and facilitates cytosolic Ca{sup 2+} oscillation upon external ATP increase, and further suggests possible role of nuclear IP{sub 3}R1 in atrial hypertrophy.

60 APPLIED LIFE SCIENCES↗