Role of inositol 1,4,5-trisphosphate receptor type 1 in ATP-induced nuclear Ca2+ signal and hypertrophy in atrial myocytes
Inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) is expressed in atrial muscle, but not in ventricle, and they are abundant in the perinucleus. We investigated the role of IP3R1 in the regulations of local Ca2+ signal and cell size in HL-1 atrial myocytes under stimulation by IP3-generating chem...
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| Published in | Biochemical and biophysical research communications Vol. 503; no. 4; pp. 2998 - 3002 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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United States
Elsevier Inc
18.09.2018
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| Online Access | Get full text |
| ISSN | 0006-291X 1090-2104 1090-2104 |
| DOI | 10.1016/j.bbrc.2018.08.084 |
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| Abstract | Inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) is expressed in atrial muscle, but not in ventricle, and they are abundant in the perinucleus. We investigated the role of IP3R1 in the regulations of local Ca2+ signal and cell size in HL-1 atrial myocytes under stimulation by IP3-generating chemical messenger, ATP. Assessment of nuclear and cytosolic Ca2+ signal using confocal Ca2+ imaging revealed that IP3 generation by ATP (1 mM) induced monophasic nuclear Ca2+ increase, followed by cytosolic Ca2+ oscillation. Genetic knock-down (KD) of IP3R1 eliminated the monophasic nuclear Ca2+ signal and slowed the cytosolic Ca2+ 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 IP3R1 KD cells. Our data indicate that IP3R1 mediates sustained elevation in nuclear Ca2+ level and facilitates cytosolic Ca2+ oscillation upon external ATP increase, and further suggests possible role of nuclear IP3R1 in atrial hypertrophy.
•IP3 receptor type 1 (IP3R1) are expressed in atrial cell perinucleus.•IP3R1 mediates ATP-induced sustained nuclear Ca2+ increase in HL-1 atrial cells.•IP3R1 contributes to higher sensitivity of nuclear release sites upon IP3 increase.•Larger Ca2+ content in perinuclear store of atrial cells involves IP3R1.•IP3R1 signaling may play a role in ATP-induced atrial cell hypertrophy. |
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| AbstractList | Inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) is expressed in atrial muscle, but not in ventricle, and they are abundant in the perinucleus. We investigated the role of IP3R1 in the regulations of local Ca2+ signal and cell size in HL-1 atrial myocytes under stimulation by IP3-generating chemical messenger, ATP. Assessment of nuclear and cytosolic Ca2+ signal using confocal Ca2+ imaging revealed that IP3 generation by ATP (1 mM) induced monophasic nuclear Ca2+ increase, followed by cytosolic Ca2+ oscillation. Genetic knock-down (KD) of IP3R1 eliminated the monophasic nuclear Ca2+ signal and slowed the cytosolic Ca2+ 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 IP3R1 KD cells. Our data indicate that IP3R1 mediates sustained elevation in nuclear Ca2+ level and facilitates cytosolic Ca2+ oscillation upon external ATP increase, and further suggests possible role of nuclear IP3R1 in atrial hypertrophy.Inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) is expressed in atrial muscle, but not in ventricle, and they are abundant in the perinucleus. We investigated the role of IP3R1 in the regulations of local Ca2+ signal and cell size in HL-1 atrial myocytes under stimulation by IP3-generating chemical messenger, ATP. Assessment of nuclear and cytosolic Ca2+ signal using confocal Ca2+ imaging revealed that IP3 generation by ATP (1 mM) induced monophasic nuclear Ca2+ increase, followed by cytosolic Ca2+ oscillation. Genetic knock-down (KD) of IP3R1 eliminated the monophasic nuclear Ca2+ signal and slowed the cytosolic Ca2+ 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 IP3R1 KD cells. Our data indicate that IP3R1 mediates sustained elevation in nuclear Ca2+ level and facilitates cytosolic Ca2+ oscillation upon external ATP increase, and further suggests possible role of nuclear IP3R1 in atrial hypertrophy. Inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) is expressed in atrial muscle, but not in ventricle, and they are abundant in the perinucleus. We investigated the role of IP3R1 in the regulations of local Ca2+ signal and cell size in HL-1 atrial myocytes under stimulation by IP3-generating chemical messenger, ATP. Assessment of nuclear and cytosolic Ca2+ signal using confocal Ca2+ imaging revealed that IP3 generation by ATP (1 mM) induced monophasic nuclear Ca2+ increase, followed by cytosolic Ca2+ oscillation. Genetic knock-down (KD) of IP3R1 eliminated the monophasic nuclear Ca2+ signal and slowed the cytosolic Ca2+ 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 IP3R1 KD cells. Our data indicate that IP3R1 mediates sustained elevation in nuclear Ca2+ level and facilitates cytosolic Ca2+ oscillation upon external ATP increase, and further suggests possible role of nuclear IP3R1 in atrial hypertrophy. •IP3 receptor type 1 (IP3R1) are expressed in atrial cell perinucleus.•IP3R1 mediates ATP-induced sustained nuclear Ca2+ increase in HL-1 atrial cells.•IP3R1 contributes to higher sensitivity of nuclear release sites upon IP3 increase.•Larger Ca2+ content in perinuclear store of atrial cells involves IP3R1.•IP3R1 signaling may play a role in ATP-induced atrial cell hypertrophy. 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. Inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) is expressed in atrial muscle, but not in ventricle, and they are abundant in the perinucleus. We investigated the role of IP3R1 in the regulations of local Ca²⁺ signal and cell size in HL-1 atrial myocytes under stimulation by IP3-generating chemical messenger, ATP. Assessment of nuclear and cytosolic Ca²⁺ signal using confocal Ca²⁺ imaging revealed that IP3 generation by ATP (1 mM) induced monophasic nuclear Ca²⁺ increase, followed by cytosolic Ca²⁺ oscillation. Genetic knock-down (KD) of IP3R1 eliminated the monophasic nuclear Ca²⁺ signal and slowed the cytosolic Ca²⁺ 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 IP3R1 KD cells. Our data indicate that IP3R1 mediates sustained elevation in nuclear Ca²⁺ level and facilitates cytosolic Ca²⁺ oscillation upon external ATP increase, and further suggests possible role of nuclear IP3R1 in atrial hypertrophy. |
| Author | Son, Min-Jeong Woo, Sun-Hee Le, Qui Anh Kim, Joon-Chul |
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| Keywords | IP3R1 IP3R2 F RyR ROI Atrial myocytes SDS-PAGE ET-1 Tp,90 PE NE KD Nuclear Ca2 ATP RFP WT Hypertrophy SR |
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| Snippet | Inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) is expressed in atrial muscle, but not in ventricle, and they are abundant in the perinucleus. We... 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+}... |
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| SubjectTerms | 60 APPLIED LIFE SCIENCES adenosine triphosphate agonists ATP Atrial myocytes calcium CALCIUM IONS calcium signaling ENDOTHELINS HEART Hypertrophy image analysis INOSITOL IP3R1 MUSCLES myocytes Nuclear Ca2 phenylephrine |
| Title | Role of inositol 1,4,5-trisphosphate receptor type 1 in ATP-induced nuclear Ca2+ signal and hypertrophy in atrial myocytes |
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