Attenuated β-adrenergic response in calcium/calmodulin-dependent protein kinase IV-knockout mice.


Journal

PloS one
ISSN: 1932-6203
Titre abrégé: PLoS One
Pays: United States
ID NLM: 101285081

Informations de publication

Date de publication:
2021
Historique:
received: 28 08 2020
accepted: 26 03 2021
entrez: 15 4 2021
pubmed: 16 4 2021
medline: 29 9 2021
Statut: epublish

Résumé

In the present study, we examined the importance of Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) in the regulation of cardiac function using genetically modified CaMKIV-null mice. RT-PCR analysis revealed decreased expression of voltage-dependent calcium channels in the cardiac myocytes of CaMKIV-null mice compared with wild-type mice. CaMKIV-null mice showed shortened QT time on electrocardiograms. Pharmacological analysis revealed decreased responsiveness to the β-adrenergic blocker propranolol in CaMKIV-null mice, whereas the plasma norepinephrine level was not affected. CaMKIV-null mice showed decreased baroreflex on electrocardiograms. Heart rate variability analysis showed unstable R-R intervals, a decreased low frequency power/high frequency power (LF/HF) ratio, and increased standard deviation of the normal to normal R-R intervals (SDNN) in CaMKIV-null mice, suggesting decreased responsiveness to β-adrenergic stimulation in CaMKIV-null mice. Atrial contraction analysis and cardiac action potential recording showed a decreased response to the β-adrenoceptor agonist isoproterenol in CaMKIV-null mice. Furthermore, fluorescence imaging in a CRE-hrGFP assay revealed a decreased response to isoproterenol in CaMKIV-null cardiac myocytes. Taken together, our data strongly suggest a significant effect of CaMKIV gene ablation on cardiac β-adrenergic signal transduction.

Identifiants

pubmed: 33857227
doi: 10.1371/journal.pone.0249932
pii: PONE-D-20-27116
pmc: PMC8049319
doi:

Substances chimiques

Adrenergic beta-Agonists 0
Adrenergic beta-Antagonists 0
Calcium Channels 0
Propranolol 9Y8NXQ24VQ
Calcium-Calmodulin-Dependent Protein Kinase Type 4 EC 2.7.11.17
Isoproterenol L628TT009W

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e0249932

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Manabu Murakami (M)

Department of Pharmacology, Graduate School of Medicine, Hirosaki University, Hirosaki, Japan.

Agnieszka M Murakami (AM)

Department of Pharmacology, Graduate School of Medicine, Hirosaki University, Hirosaki, Japan.

Yasushi Matsuzaki (Y)

Department of Dermatology, Graduate School of Medicine, Hirosaki University, Hirosaki, Japan.

Daisuke Sawamura (D)

Department of Dermatology, Graduate School of Medicine, Hirosaki University, Hirosaki, Japan.

Takayoshi Ohba (T)

Department of Cell Physiology, Akita University School of Medicine, Akita, Japan.

Ichirou Miyoshi (I)

Department of Animal Care, Tohoku University School of Medicine, Aoba-Ku, Sendai, Japan.

Shirou Itagaki (S)

Collaboration Center for Community and Industry, Sapporo Medical University, Sapporo, Japan.

Hiroyuki Sakagami (H)

Department of Anatomy, Kitasato University School of Medicine, Sagamihara, Japan.

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Classifications MeSH