Enhanced β-adrenergic response in mice with dominant-negative expression of the PKD2L1 channel
Polycystic kidney disease (PKD) is the most common genetic cause of kidney failure in humans. Among the various PKD-related molecules, PKD2L1 forms cation channels, but its physiological importance is obscure. In the present study, we established a transgenic mouse line by overexpressing the dominant-negative form of the mouse PKD2L1 gene (i.e., lacking the pore-forming domain). The resulting PKD2L1del-Tg mice exhibited supraventricular premature contraction, as well as enhanced sensitivity to β-adrenergic stimulation and unstable R-R intervals in electrocardiography. During spontaneous atrial contraction, PKD2L1del-Tg atria showed enhanced sensitivity to isoproterenol, norepinephrine, and epinephrine. Action potential recording revealed a shortened action potential duration in PKD2L1del-Tg atria in response to isoproterenol. These findings indicated increased adrenergic sensitivity in PKD2L1del-Tg mice, suggesting that PKD2L1 is involved in sympathetic regulation.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2022 |
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| Erschienen: |
2022 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:17 |
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| Enthalten in: |
PloS one - 17(2022), 1 vom: 21., Seite e0261668 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Murakami, Manabu [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 10.02.2022 Date Revised 10.02.2022 published: Electronic-eCollection Citation Status MEDLINE |
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| doi: |
10.1371/journal.pone.0261668 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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NLM335858368 |
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| 245 | 1 | 0 | |a Enhanced β-adrenergic response in mice with dominant-negative expression of the PKD2L1 channel |
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| 520 | |a Polycystic kidney disease (PKD) is the most common genetic cause of kidney failure in humans. Among the various PKD-related molecules, PKD2L1 forms cation channels, but its physiological importance is obscure. In the present study, we established a transgenic mouse line by overexpressing the dominant-negative form of the mouse PKD2L1 gene (i.e., lacking the pore-forming domain). The resulting PKD2L1del-Tg mice exhibited supraventricular premature contraction, as well as enhanced sensitivity to β-adrenergic stimulation and unstable R-R intervals in electrocardiography. During spontaneous atrial contraction, PKD2L1del-Tg atria showed enhanced sensitivity to isoproterenol, norepinephrine, and epinephrine. Action potential recording revealed a shortened action potential duration in PKD2L1del-Tg atria in response to isoproterenol. These findings indicated increased adrenergic sensitivity in PKD2L1del-Tg mice, suggesting that PKD2L1 is involved in sympathetic regulation | ||
| 650 | 4 | |a Journal Article | |
| 650 | 7 | |a Calcium Channels |2 NLM | |
| 700 | 1 | |a Murakami, Agnieszka M |e verfasserin |4 aut | |
| 700 | 1 | |a Nemoto, Takayuki |e verfasserin |4 aut | |
| 700 | 1 | |a Ohba, Takayoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Yonekura, Manabu |e verfasserin |4 aut | |
| 700 | 1 | |a Toyama, Yuichi |e verfasserin |4 aut | |
| 700 | 1 | |a Tomita, Hirofumi |e verfasserin |4 aut | |
| 700 | 1 | |a Matsuzaki, Yasushi |e verfasserin |4 aut | |
| 700 | 1 | |a Sawamura, Daisuke |e verfasserin |4 aut | |
| 700 | 1 | |a Hirota, Kazuyoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Itagaki, Shirou |e verfasserin |4 aut | |
| 700 | 1 | |a Asada, Yujiro |e verfasserin |4 aut | |
| 700 | 1 | |a Miyoshi, Ichiro |e verfasserin |4 aut | |
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