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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 |
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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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-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.</description><identifier>ISSN: 1880-6562</identifier><identifier>ISSN: 1880-6546</identifier><identifier>EISSN: 1880-6562</identifier><identifier>DOI: 10.1186/s12576-023-00873-5</identifier><identifier>PMID: 37558983</identifier><language>eng</language><publisher>Japan: Springer</publisher><subject>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</subject><ispartof>The journal of physiological sciences, 2023-08, Vol.73 (1), p.18-18, Article 18</ispartof><rights>2023. The Physiological Society of Japan.</rights><rights>COPYRIGHT 2023 Springer</rights><rights>2023. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>The Author(s) 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c577t-8212ef2d302a446d04a8ca4175a2d4b9aae3a27e07e30348c21325d80a0425de3</cites><orcidid>0000-0001-8747-7941</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2849919185/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2849919185?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37558983$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsunoda, Michinori</creatorcontrib><creatorcontrib>Matsuo, Ichiro</creatorcontrib><creatorcontrib>Ohnuki, Yoshiki</creatorcontrib><creatorcontrib>Suita, Kenji</creatorcontrib><creatorcontrib>Ishikawa, Misao</creatorcontrib><creatorcontrib>Mitsubayashi, Takao</creatorcontrib><creatorcontrib>Ito, Aiko</creatorcontrib><creatorcontrib>Mototani, Yasumasa</creatorcontrib><creatorcontrib>Kiyomoto, Kenichi</creatorcontrib><creatorcontrib>Morii, Akinaka</creatorcontrib><creatorcontrib>Nariyama, Megumi</creatorcontrib><creatorcontrib>Hayakawa, Yoshio</creatorcontrib><creatorcontrib>Gomi, Kazuhiro</creatorcontrib><creatorcontrib>Okumura, Satoshi</creatorcontrib><title>Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice</title><title>The journal of physiological sciences</title><addtitle>J Physiol Sci</addtitle><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.</description><subject>Adenylate cyclase</subject><subject>Adenylyl cyclase</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Ca2+/calmodulin-dependent protein kinase II</subject><subject>Calmodulin</subject><subject>Cardiac function</subject><subject>Cardiomyopathies</subject><subject>Cardiovascular diseases</subject><subject>Cellular signal transduction</subject><subject>Drug dosages</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Fibrosis</subject><subject>Frailty</subject><subject>Heart</subject><subject>Heart failure</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - toxicity</subject><subject>Mice</subject><subject>Mortality</subject><subject>Myocytes</subject><subject>Oral hygiene</subject><subject>Original Paper</subject><subject>Periodontitis</subject><subject>Phospholamban</subject><subject>Phosphorylation</subject><subject>Porphyromonas gingivalis</subject><subject>Protein kinases</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Threonine</subject><subject>Vidarabine</subject><subject>β-Adrenergic signaling</subject><issn>1880-6562</issn><issn>1880-6546</issn><issn>1880-6562</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptUktv1DAQjhCIlsIf4IAiceHQFL8Se0-oqnhUqgQH4GpN7EnWq8QOdrLS8uvxdkvposqWxh5_83keX1G8puSCUtW8T5TVsqkI4xUhSvKqflKcUqVI1dQNe_rgfFK8SGlDiGhWTD0vTrisa7VS_LT4_dNZiNA6j-cl-LxnV60xTphK6NHP56Ubpxi2-f4txGm9i2EMHlLZO9-7LQwulYObwhSGXQJj1hCdxcp5uxi0pYFoHZjS7lK3eDO74Evny9EZfFk862BI-OrOnhU_Pn38fvWluvn6-frq8qYytZRzpRhl2DHLCQMhGksEKAOCyhqYFe0KADkwiUQiJ1wowyhntVUEiMgW-VlxfeC1ATZ6im6EuNMBnL51hNhriLMzA-qGtIAgedfYTqCxiluoOzBtLgW7rs1cHw5c09KOaE1uUIThiPT4xbu17sNWUyKpJFJlhnd3DDH8WjDNenTJ4DCAx7AkzZRQSgghSYa-_Q-6CUv0uVd71GpFV1TV_1A95Aqc70L-2OxJ9aVsCJON4iyjqkdQecCYswweO5fdR_iLR_B5WcyzezSAHQJMDClF7O6bQoney1Uf5KqzXPWtXPU-9zcP23kf8lef_A9LLufn</recordid><startdate>20230809</startdate><enddate>20230809</enddate><creator>Tsunoda, Michinori</creator><creator>Matsuo, Ichiro</creator><creator>Ohnuki, Yoshiki</creator><creator>Suita, Kenji</creator><creator>Ishikawa, Misao</creator><creator>Mitsubayashi, Takao</creator><creator>Ito, Aiko</creator><creator>Mototani, Yasumasa</creator><creator>Kiyomoto, Kenichi</creator><creator>Morii, Akinaka</creator><creator>Nariyama, Megumi</creator><creator>Hayakawa, Yoshio</creator><creator>Gomi, Kazuhiro</creator><creator>Okumura, Satoshi</creator><general>Springer</general><general>BioMed Central</general><general>BMC</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-8747-7941</orcidid></search><sort><creationdate>20230809</creationdate><title>Vidarabine, an anti-herpes agent, improves Porphyromonas gingivalis lipopolysaccharide-induced cardiac dysfunction in mice</title><author>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</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c577t-8212ef2d302a446d04a8ca4175a2d4b9aae3a27e07e30348c21325d80a0425de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adenylate cyclase</topic><topic>Adenylyl cyclase</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Ca2+/calmodulin-dependent protein kinase II</topic><topic>Calmodulin</topic><topic>Cardiac function</topic><topic>Cardiomyopathies</topic><topic>Cardiovascular diseases</topic><topic>Cellular signal transduction</topic><topic>Drug dosages</topic><topic>Ethylenediaminetetraacetic acid</topic><topic>Fibrosis</topic><topic>Frailty</topic><topic>Heart</topic><topic>Heart failure</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - toxicity</topic><topic>Mice</topic><topic>Mortality</topic><topic>Myocytes</topic><topic>Oral hygiene</topic><topic>Original Paper</topic><topic>Periodontitis</topic><topic>Phospholamban</topic><topic>Phosphorylation</topic><topic>Porphyromonas gingivalis</topic><topic>Protein kinases</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Threonine</topic><topic>Vidarabine</topic><topic>β-Adrenergic signaling</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsunoda, Michinori</creatorcontrib><creatorcontrib>Matsuo, Ichiro</creatorcontrib><creatorcontrib>Ohnuki, Yoshiki</creatorcontrib><creatorcontrib>Suita, Kenji</creatorcontrib><creatorcontrib>Ishikawa, Misao</creatorcontrib><creatorcontrib>Mitsubayashi, Takao</creatorcontrib><creatorcontrib>Ito, Aiko</creatorcontrib><creatorcontrib>Mototani, Yasumasa</creatorcontrib><creatorcontrib>Kiyomoto, Kenichi</creatorcontrib><creatorcontrib>Morii, Akinaka</creatorcontrib><creatorcontrib>Nariyama, Megumi</creatorcontrib><creatorcontrib>Hayakawa, Yoshio</creatorcontrib><creatorcontrib>Gomi, Kazuhiro</creatorcontrib><creatorcontrib>Okumura, Satoshi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest Biological Science Journals</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - 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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. These results suggest that pharmacological AC5 inhibition may be a promising approach to treat PD-associated cardiovascular disease.</abstract><cop>Japan</cop><pub>Springer</pub><pmid>37558983</pmid><doi>10.1186/s12576-023-00873-5</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-8747-7941</orcidid><oa>free_for_read</oa></addata></record> |
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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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