Acid-sensing ion channel 3, but not capsaicin receptor TRPV1, plays a protective role in isoproterenol-induced myocardial ischemia in mice

Ching Feng Cheng, I. Lun Chen, Mei Hsin Cheng, Wei Shiung Lian, Chao Chieh Lin, Terry B.J. Kuo, Chih Cheng Chen

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Background: Cardiac angina is the hallmark of myocardial ischemia, but the role of the cardiac sensory nerve has received relatively little attention. Recently, both acid-sensing ion channel 3 (ASIC3) and capsaicin receptor (TRPV1) have been suggested as important mediators in sensing myocardial ischemia. However, studies comparing the physiological roles of ASIC3 and TRPV1 in the neuronal-cardiac sensing circuits in vivo are lacking. Methods and Results: Isoproterenol (1.5mg/kg, intraperitoneally) was used to induce transient myocardial ischemia in Asic3+/+ and Asic3-/-mice and a radio-telemetry system was used for electrocardiography with mice in a conscious state. Isoproterenol-induced myocardial ischemia was first demonstrated with ST-segment depression and further confirmed by hypoxia-mediated chemical reactions in cardiac tissue. Mice lacking Asic3 showed prolonged duration of ST-segment depression compared with Asic3+/+ mice (44.3±3.1 vs. 31.7±2.9min; P<0.05). Although ischemia was transient, severe cardiac fibrosis was found in Asic3 -/- but not in Asic3+/+ mice littermates. In contrast, isoproterenol-injected Trpv1+/+ and Trpv1 -/- mice showed no difference in duration of ST-segment depression and, surprisingly, deletion of Trpv1 did not aggravate cardiac fibrosis. Conclusions: An isoproterenol-induced myocardial ischemia model mimicking clinical conditions of early cardiac angina was used to demonstrate that ASIC3 but not TRPV1 plays a protective role in sensing myocardial ischemia.

Original languageEnglish
Pages (from-to)174-178
Number of pages5
JournalCirculation Journal
Volume75
Issue number1
DOIs
Publication statusPublished - 2011
Externally publishedYes

Fingerprint

Acid Sensing Ion Channels
TRPV Cation Channels
Isoproterenol
Myocardial Ischemia
Fibrosis
Telemetry
Radio
Electrocardiography
Ischemia

Keywords

  • Asic3
  • Electrocardiography
  • Isoproterenol
  • Myocardial ischemia
  • Trpv1

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Acid-sensing ion channel 3, but not capsaicin receptor TRPV1, plays a protective role in isoproterenol-induced myocardial ischemia in mice. / Cheng, Ching Feng; Chen, I. Lun; Cheng, Mei Hsin; Lian, Wei Shiung; Lin, Chao Chieh; Kuo, Terry B.J.; Chen, Chih Cheng.

In: Circulation Journal, Vol. 75, No. 1, 2011, p. 174-178.

Research output: Contribution to journalArticle

Cheng, Ching Feng ; Chen, I. Lun ; Cheng, Mei Hsin ; Lian, Wei Shiung ; Lin, Chao Chieh ; Kuo, Terry B.J. ; Chen, Chih Cheng. / Acid-sensing ion channel 3, but not capsaicin receptor TRPV1, plays a protective role in isoproterenol-induced myocardial ischemia in mice. In: Circulation Journal. 2011 ; Vol. 75, No. 1. pp. 174-178.
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abstract = "Background: Cardiac angina is the hallmark of myocardial ischemia, but the role of the cardiac sensory nerve has received relatively little attention. Recently, both acid-sensing ion channel 3 (ASIC3) and capsaicin receptor (TRPV1) have been suggested as important mediators in sensing myocardial ischemia. However, studies comparing the physiological roles of ASIC3 and TRPV1 in the neuronal-cardiac sensing circuits in vivo are lacking. Methods and Results: Isoproterenol (1.5mg/kg, intraperitoneally) was used to induce transient myocardial ischemia in Asic3+/+ and Asic3-/-mice and a radio-telemetry system was used for electrocardiography with mice in a conscious state. Isoproterenol-induced myocardial ischemia was first demonstrated with ST-segment depression and further confirmed by hypoxia-mediated chemical reactions in cardiac tissue. Mice lacking Asic3 showed prolonged duration of ST-segment depression compared with Asic3+/+ mice (44.3±3.1 vs. 31.7±2.9min; P<0.05). Although ischemia was transient, severe cardiac fibrosis was found in Asic3 -/- but not in Asic3+/+ mice littermates. In contrast, isoproterenol-injected Trpv1+/+ and Trpv1 -/- mice showed no difference in duration of ST-segment depression and, surprisingly, deletion of Trpv1 did not aggravate cardiac fibrosis. Conclusions: An isoproterenol-induced myocardial ischemia model mimicking clinical conditions of early cardiac angina was used to demonstrate that ASIC3 but not TRPV1 plays a protective role in sensing myocardial ischemia.",
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AU - Lin, Chao Chieh

AU - Kuo, Terry B.J.

AU - Chen, Chih Cheng

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AB - Background: Cardiac angina is the hallmark of myocardial ischemia, but the role of the cardiac sensory nerve has received relatively little attention. Recently, both acid-sensing ion channel 3 (ASIC3) and capsaicin receptor (TRPV1) have been suggested as important mediators in sensing myocardial ischemia. However, studies comparing the physiological roles of ASIC3 and TRPV1 in the neuronal-cardiac sensing circuits in vivo are lacking. Methods and Results: Isoproterenol (1.5mg/kg, intraperitoneally) was used to induce transient myocardial ischemia in Asic3+/+ and Asic3-/-mice and a radio-telemetry system was used for electrocardiography with mice in a conscious state. Isoproterenol-induced myocardial ischemia was first demonstrated with ST-segment depression and further confirmed by hypoxia-mediated chemical reactions in cardiac tissue. Mice lacking Asic3 showed prolonged duration of ST-segment depression compared with Asic3+/+ mice (44.3±3.1 vs. 31.7±2.9min; P<0.05). Although ischemia was transient, severe cardiac fibrosis was found in Asic3 -/- but not in Asic3+/+ mice littermates. In contrast, isoproterenol-injected Trpv1+/+ and Trpv1 -/- mice showed no difference in duration of ST-segment depression and, surprisingly, deletion of Trpv1 did not aggravate cardiac fibrosis. Conclusions: An isoproterenol-induced myocardial ischemia model mimicking clinical conditions of early cardiac angina was used to demonstrate that ASIC3 but not TRPV1 plays a protective role in sensing myocardial ischemia.

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