Key result
Homozygous vtg-2J mice with a Kcnq1 mutation exhibited significantly prolonged QT intervals (32.8 vs 22.7 ms), gastric achlorhydria, hypergastrinemia, elevated corticosterone, and hypertension.
Absolute Event Rate: 32.8% vs 22.7%
p-value: p=<0.05
The Kcnq1 mutation in vtg-2J mice alters cardiac, gastric, and adrenocortical functions, establishing it as a useful preclinical model for studying Kcnq1 functions and congenital long QT syndrome.
Establishes vtg-2J mice as a Kcnq1 model; leaves open human translation to congenital long QT syndrome.
The KCNQ1 gene encodes a voltage-dependent potassium ion channel, and mutations in this gene are the most common cause of congenital long QT syndrome (LQTS). In the present study, we investigated the various phenotypic characteristics of vertigo 2 Jackson (C3H/HeJCrl-Kcnq1(vtg-2J)/J) mice with a Kcnq1 mutation. Both heterozygotes (vtg-2J/+) and homozygotes (vtg-2J/vtg-2J) showed prolonged QT intervals in electrocardiograms (ECGs) compared to C3H/HeJ control (+/+) mice. Furthermore, vtg-2J/vtg-2J mice showed gastric achlorhydria associated with elevation of their serum gastrin levels. The serum corticosterone levels were also significantly increased in vtg-2J/vtg-2J mice. In addition, vtg-2J/vtg-2J mice exhibited significantly higher blood pressure. These findings indicate that the Kcnq1 mutation in vtg-2J mice alters various physiological functions in the cardiac, gastric and adrenocortical systems, and suggest that vtg-2J mice may represent a useful model for studying Kcnq1 functions.
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Takagi et al. (2007) studied Long QT syndrome (Kcnq1 mutation). Kcnq1 mutation (vtg-2J allele) vs. Wild-type C3H/HeJ mice (+/+) was evaluated on QT interval (ms) (p=<0.05). Homozygous vtg-2J mice with a Kcnq1 mutation exhibited significantly prolonged QT intervals (32.8 vs 22.7 ms), gastric achlorhydria, hypergastrinemia, elevated corticosterone, and hypertension.
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