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
Format: Article
Language:English
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
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Summary: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.
ISSN:1880-6562
1880-6546
1880-6562
DOI:10.1186/s12576-023-00873-5