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Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice

In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in...

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Published in:The journal of physiological sciences 2023-08, Vol.73 (1), p.18-18, Article 18
Main Authors: Tsunoda, Michinori, Matsuo, Ichiro, Ohnuki, Yoshiki, Suita, Kenji, Ishikawa, Misao, Mitsubayashi, Takao, Ito, Aiko, Mototani, Yasumasa, Kiyomoto, Kenichi, Morii, Akinaka, Nariyama, Megumi, Hayakawa, Yoshio, Gomi, Kazuhiro, Okumura, Satoshi
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container_title The journal of physiological sciences
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creator Tsunoda, Michinori
Matsuo, Ichiro
Ohnuki, Yoshiki
Suita, Kenji
Ishikawa, Misao
Mitsubayashi, Takao
Ito, Aiko
Mototani, Yasumasa
Kiyomoto, Kenichi
Morii, Akinaka
Nariyama, Megumi
Hayakawa, Yoshio
Gomi, Kazuhiro
Okumura, Satoshi
description In this work, we examined the involvement of type 5 adenylyl cyclase (AC5) in cardiac dysfunction induced in mice given Porphyromonas gingivalis lipopolysaccharide (PG-LPS) at a dose equivalent to the circulating levels in periodontitis (PD) patients. Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/Ca -calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease.
doi_str_mv 10.1186/s12576-023-00873-5
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Cardiac function was significantly decreased in mice given PG-LPS compared to the control, but treatment for 1 week with the AC5 inhibitor vidarabine ameliorated the dysfunction. Cardiac fibrosis and myocyte apoptosis were significantly increased in the PG-LPS group, but vidarabine blocked these changes. The PG-LPS-induced cardiac dysfunction was associated with activation of cyclic AMP/Ca -calmodulin-dependent protein kinase II signaling and increased phospholamban phosphorylation at threonine 17. 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ispartof The journal of physiological sciences, 2023-08, Vol.73 (1), p.18-18, Article 18
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subjects Adenylate cyclase
Adenylyl cyclase
Animals
Apoptosis
Ca2+/calmodulin-dependent protein kinase II
Calmodulin
Cardiac function
Cardiomyopathies
Cardiovascular diseases
Cellular signal transduction
Drug dosages
Ethylenediaminetetraacetic acid
Fibrosis
Frailty
Heart
Heart failure
Kinases
Laboratory animals
Lipopolysaccharides
Lipopolysaccharides - toxicity
Mice
Mortality
Myocytes
Oral hygiene
Original Paper
Periodontitis
Phospholamban
Phosphorylation
Porphyromonas gingivalis
Protein kinases
Proteins
Signal transduction
Threonine
Vidarabine
β-Adrenergic signaling
title Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice
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