Effect of butyrate, a bacterial by‐product, on the viability and ICAM‐1 expression/production of human vascular endothelial cells: Role in infectious pulpal/periapical diseases
Aim To investigate the effects of butyric acid (BA), a metabolic product generated by pulp and root canal pathogens, on the viability and intercellular adhesion molecule‐1 (ICAM‐1) production of endothelial cells, which are crucial to angiogenesis and pulpal/periapical wound healing. Methodology End...
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| Veröffentlicht in: | International endodontic journal 2022-01, Vol.55 (1), p.38-53 |
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| creator | Chang, Mei‐Chi Wang, Tong‐Mei Chien, Hua‐Hong Pan, Yu‐Hwa Tsai, Yi‐Ling Jeng, Po‐Yuan Lin, Li‐Deh Jeng, Jiiang‐Huei |
| description | Aim
To investigate the effects of butyric acid (BA), a metabolic product generated by pulp and root canal pathogens, on the viability and intercellular adhesion molecule‐1 (ICAM‐1) production of endothelial cells, which are crucial to angiogenesis and pulpal/periapical wound healing.
Methodology
Endothelial cells were exposed to butyrate with/without inhibitors. Cell viability, apoptosis and reactive oxygen species (ROS) were evaluated using an MTT assay, PI/annexin V and DCF fluorescence flow cytometry respectively. RNA and protein expression was determined using a polymerase chain reaction assay and Western blotting or immunofluorescent staining. Soluble ICAM‐1 (sICAM‐1) was measured using an enzyme‐linked immunosorbent assay. The quantitative results were expressed as mean ± standard error (SE) of the mean. The data were analysed using a paired Student's t‐test where necessary. A p‐value ≤0.05 was considered to indicate a statistically significant difference between groups.
Results
Butyrate (>4 mM) inhibited cell viability and induced cellular apoptosis and necrosis. It inhibited cyclin B1 but stimulated p21 and p27 expression. Butyrate stimulated ROS production and hemeoxygenase‐1 (HO‐1) expression as well as activated the Ac‐H3, p‐ATM, p‐ATR, p‐Chk1, p‐Chk2, p‐p38 and p‐Akt expression of endothelial cells. Butyrate stimulated ICAM‐1 mRNA/protein expression and significant sICAM‐1 production (p |
| doi_str_mv | 10.1111/iej.13614 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2563697455</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2563697455</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3534-bf0bc4897abcfe74bb8fc324b5a46e0dbc539221b1c968d0355f57d67ac8afa93</originalsourceid><addsrcrecordid>eNp1kd-K1DAUh4Mo7rh64QtIwBuF7U7-dlrvZBl1ZUUQvS4n6QmbIdPWpF23d_sIPoxP5JOYOqMXgiFwcvHl43f4EfKUs3Oez9rj7pzLkqt7ZJWnLoSu-X2yYlzJQlSVPiGPUtoxxjST_CE5kUoJJgRbkR9b59COtHfUTOMcYcQzCtSAHTF6CNTMP---D7FvJzue0b6j4zXSGw_GBz_OFLqWXl68_pAhTvF2iJiS77v18Ud-LurraQ8dvYFkpwCRYtf2WRMWv8UQ0iv6qQ9IfZfvEsf3U6LDFAYI62HJMXib2dYnhITpMXngICR8cpyn5Mub7eeLd8XVx7c5zFVhpZaqMI4Zq6p6A8Y63ChjKmelUEaDKpG1xmpZC8ENt3VZtUxq7fSmLTdgK3BQy1Py4uDN23ydMI3N3qclMHSYEzZCl7KsN0rrjD7_B931U-xyukaUrGJZrmSmXh4oG_uUIrpmiH4PcW44a5Yqm1xl87vKzD47Giezx_Yv-ae7DKwPwDcfcP6_qbncvj8ofwH-LK0B</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2608003543</pqid></control><display><type>article</type><title>Effect of butyrate, a bacterial by‐product, on the viability and ICAM‐1 expression/production of human vascular endothelial cells: Role in infectious pulpal/periapical diseases</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Chang, Mei‐Chi ; Wang, Tong‐Mei ; Chien, Hua‐Hong ; Pan, Yu‐Hwa ; Tsai, Yi‐Ling ; Jeng, Po‐Yuan ; Lin, Li‐Deh ; Jeng, Jiiang‐Huei</creator><creatorcontrib>Chang, Mei‐Chi ; Wang, Tong‐Mei ; Chien, Hua‐Hong ; Pan, Yu‐Hwa ; Tsai, Yi‐Ling ; Jeng, Po‐Yuan ; Lin, Li‐Deh ; Jeng, Jiiang‐Huei</creatorcontrib><description>Aim
To investigate the effects of butyric acid (BA), a metabolic product generated by pulp and root canal pathogens, on the viability and intercellular adhesion molecule‐1 (ICAM‐1) production of endothelial cells, which are crucial to angiogenesis and pulpal/periapical wound healing.
Methodology
Endothelial cells were exposed to butyrate with/without inhibitors. Cell viability, apoptosis and reactive oxygen species (ROS) were evaluated using an MTT assay, PI/annexin V and DCF fluorescence flow cytometry respectively. RNA and protein expression was determined using a polymerase chain reaction assay and Western blotting or immunofluorescent staining. Soluble ICAM‐1 (sICAM‐1) was measured using an enzyme‐linked immunosorbent assay. The quantitative results were expressed as mean ± standard error (SE) of the mean. The data were analysed using a paired Student's t‐test where necessary. A p‐value ≤0.05 was considered to indicate a statistically significant difference between groups.
Results
Butyrate (>4 mM) inhibited cell viability and induced cellular apoptosis and necrosis. It inhibited cyclin B1 but stimulated p21 and p27 expression. Butyrate stimulated ROS production and hemeoxygenase‐1 (HO‐1) expression as well as activated the Ac‐H3, p‐ATM, p‐ATR, p‐Chk1, p‐Chk2, p‐p38 and p‐Akt expression of endothelial cells. Butyrate stimulated ICAM‐1 mRNA/protein expression and significant sICAM‐1 production (p < .05). Superoxide dismutase, 5z‐7oxozeaenol, SB203580 and compound C (p < .05), but not ZnPP, CGK733, AZD7762 or LY294002, attenuated butyrate cytotoxicity to endothelial cells. Notably, little effect on butyrate‐stimulated sICAM‐1 secretion was found. Valproic acid, phenylbutyrate and trichostatin (three histone deacetylase inhibitors) significantly induced sICAM‐1 production (p < .05).
Conclusion
Butyric acid inhibited proliferation, induced apoptosis, stimulated ROS and HO‐1 production and increased ICAM‐1 mRNA expression and protein synthesis in endothelial cells. Cell viability affected by BA was diminished by some inhibitors; however, the increased sICAM‐1 secretion by BA was not affected by any of the tested inhibitors. These results facilitate understanding of the pathogenesis, prevention and treatment of pulpal/periapical diseases.</description><identifier>ISSN: 0143-2885</identifier><identifier>EISSN: 1365-2591</identifier><identifier>DOI: 10.1111/iej.13614</identifier><identifier>PMID: 34420220</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>AKT protein ; Angiogenesis ; Annexin V ; apical periodontitis ; Apoptosis ; Butyric acid ; Butyric Acid - pharmacology ; Cell adhesion ; Cell viability ; Cells, Cultured ; CHK1 protein ; Cyclin B1 ; Cytotoxicity ; Dental Pulp - cytology ; Endothelial cells ; Endothelial Cells - metabolism ; Flow cytometry ; Gene expression ; Gum disease ; Histone deacetylase ; Humans ; Intercellular Adhesion Molecule-1 - metabolism ; intercellular cell adhesion molecule‐1 ; Periapical Diseases ; Phenylbutyric acid ; Polymerase chain reaction ; Protein biosynthesis ; Protein expression ; Proteins ; Reactive oxygen species ; risk factors for cardiovascular disease ; Root canals ; signal transduction pathways ; Statistical analysis ; Superoxide dismutase ; Transcription ; Valproic acid ; Western blotting ; Wound healing</subject><ispartof>International endodontic journal, 2022-01, Vol.55 (1), p.38-53</ispartof><rights>2021 International Endodontic Journal. Published by John Wiley & Sons Ltd</rights><rights>2021 International Endodontic Journal. Published by John Wiley & Sons Ltd.</rights><rights>Copyright © 2022 International Endodontic Journal. Published by John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3534-bf0bc4897abcfe74bb8fc324b5a46e0dbc539221b1c968d0355f57d67ac8afa93</citedby><cites>FETCH-LOGICAL-c3534-bf0bc4897abcfe74bb8fc324b5a46e0dbc539221b1c968d0355f57d67ac8afa93</cites><orcidid>0000-0002-2068-5380</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fiej.13614$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fiej.13614$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34420220$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chang, Mei‐Chi</creatorcontrib><creatorcontrib>Wang, Tong‐Mei</creatorcontrib><creatorcontrib>Chien, Hua‐Hong</creatorcontrib><creatorcontrib>Pan, Yu‐Hwa</creatorcontrib><creatorcontrib>Tsai, Yi‐Ling</creatorcontrib><creatorcontrib>Jeng, Po‐Yuan</creatorcontrib><creatorcontrib>Lin, Li‐Deh</creatorcontrib><creatorcontrib>Jeng, Jiiang‐Huei</creatorcontrib><title>Effect of butyrate, a bacterial by‐product, on the viability and ICAM‐1 expression/production of human vascular endothelial cells: Role in infectious pulpal/periapical diseases</title><title>International endodontic journal</title><addtitle>Int Endod J</addtitle><description>Aim
To investigate the effects of butyric acid (BA), a metabolic product generated by pulp and root canal pathogens, on the viability and intercellular adhesion molecule‐1 (ICAM‐1) production of endothelial cells, which are crucial to angiogenesis and pulpal/periapical wound healing.
Methodology
Endothelial cells were exposed to butyrate with/without inhibitors. Cell viability, apoptosis and reactive oxygen species (ROS) were evaluated using an MTT assay, PI/annexin V and DCF fluorescence flow cytometry respectively. RNA and protein expression was determined using a polymerase chain reaction assay and Western blotting or immunofluorescent staining. Soluble ICAM‐1 (sICAM‐1) was measured using an enzyme‐linked immunosorbent assay. The quantitative results were expressed as mean ± standard error (SE) of the mean. The data were analysed using a paired Student's t‐test where necessary. A p‐value ≤0.05 was considered to indicate a statistically significant difference between groups.
Results
Butyrate (>4 mM) inhibited cell viability and induced cellular apoptosis and necrosis. It inhibited cyclin B1 but stimulated p21 and p27 expression. Butyrate stimulated ROS production and hemeoxygenase‐1 (HO‐1) expression as well as activated the Ac‐H3, p‐ATM, p‐ATR, p‐Chk1, p‐Chk2, p‐p38 and p‐Akt expression of endothelial cells. Butyrate stimulated ICAM‐1 mRNA/protein expression and significant sICAM‐1 production (p < .05). Superoxide dismutase, 5z‐7oxozeaenol, SB203580 and compound C (p < .05), but not ZnPP, CGK733, AZD7762 or LY294002, attenuated butyrate cytotoxicity to endothelial cells. Notably, little effect on butyrate‐stimulated sICAM‐1 secretion was found. Valproic acid, phenylbutyrate and trichostatin (three histone deacetylase inhibitors) significantly induced sICAM‐1 production (p < .05).
Conclusion
Butyric acid inhibited proliferation, induced apoptosis, stimulated ROS and HO‐1 production and increased ICAM‐1 mRNA expression and protein synthesis in endothelial cells. Cell viability affected by BA was diminished by some inhibitors; however, the increased sICAM‐1 secretion by BA was not affected by any of the tested inhibitors. These results facilitate understanding of the pathogenesis, prevention and treatment of pulpal/periapical diseases.</description><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Annexin V</subject><subject>apical periodontitis</subject><subject>Apoptosis</subject><subject>Butyric acid</subject><subject>Butyric Acid - pharmacology</subject><subject>Cell adhesion</subject><subject>Cell viability</subject><subject>Cells, Cultured</subject><subject>CHK1 protein</subject><subject>Cyclin B1</subject><subject>Cytotoxicity</subject><subject>Dental Pulp - cytology</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - metabolism</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Gum disease</subject><subject>Histone deacetylase</subject><subject>Humans</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>intercellular cell adhesion molecule‐1</subject><subject>Periapical Diseases</subject><subject>Phenylbutyric acid</subject><subject>Polymerase chain reaction</subject><subject>Protein biosynthesis</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>risk factors for cardiovascular disease</subject><subject>Root canals</subject><subject>signal transduction pathways</subject><subject>Statistical analysis</subject><subject>Superoxide dismutase</subject><subject>Transcription</subject><subject>Valproic acid</subject><subject>Western blotting</subject><subject>Wound healing</subject><issn>0143-2885</issn><issn>1365-2591</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kd-K1DAUh4Mo7rh64QtIwBuF7U7-dlrvZBl1ZUUQvS4n6QmbIdPWpF23d_sIPoxP5JOYOqMXgiFwcvHl43f4EfKUs3Oez9rj7pzLkqt7ZJWnLoSu-X2yYlzJQlSVPiGPUtoxxjST_CE5kUoJJgRbkR9b59COtHfUTOMcYcQzCtSAHTF6CNTMP---D7FvJzue0b6j4zXSGw_GBz_OFLqWXl68_pAhTvF2iJiS77v18Ud-LurraQ8dvYFkpwCRYtf2WRMWv8UQ0iv6qQ9IfZfvEsf3U6LDFAYI62HJMXib2dYnhITpMXngICR8cpyn5Mub7eeLd8XVx7c5zFVhpZaqMI4Zq6p6A8Y63ChjKmelUEaDKpG1xmpZC8ENt3VZtUxq7fSmLTdgK3BQy1Py4uDN23ydMI3N3qclMHSYEzZCl7KsN0rrjD7_B931U-xyukaUrGJZrmSmXh4oG_uUIrpmiH4PcW44a5Yqm1xl87vKzD47Giezx_Yv-ae7DKwPwDcfcP6_qbncvj8ofwH-LK0B</recordid><startdate>202201</startdate><enddate>202201</enddate><creator>Chang, Mei‐Chi</creator><creator>Wang, Tong‐Mei</creator><creator>Chien, Hua‐Hong</creator><creator>Pan, Yu‐Hwa</creator><creator>Tsai, Yi‐Ling</creator><creator>Jeng, Po‐Yuan</creator><creator>Lin, Li‐Deh</creator><creator>Jeng, Jiiang‐Huei</creator><general>Wiley Subscription Services, Inc</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>7QP</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-2068-5380</orcidid></search><sort><creationdate>202201</creationdate><title>Effect of butyrate, a bacterial by‐product, on the viability and ICAM‐1 expression/production of human vascular endothelial cells: Role in infectious pulpal/periapical diseases</title><author>Chang, Mei‐Chi ; Wang, Tong‐Mei ; Chien, Hua‐Hong ; Pan, Yu‐Hwa ; Tsai, Yi‐Ling ; Jeng, Po‐Yuan ; Lin, Li‐Deh ; Jeng, Jiiang‐Huei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3534-bf0bc4897abcfe74bb8fc324b5a46e0dbc539221b1c968d0355f57d67ac8afa93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>AKT protein</topic><topic>Angiogenesis</topic><topic>Annexin V</topic><topic>apical periodontitis</topic><topic>Apoptosis</topic><topic>Butyric acid</topic><topic>Butyric Acid - pharmacology</topic><topic>Cell adhesion</topic><topic>Cell viability</topic><topic>Cells, Cultured</topic><topic>CHK1 protein</topic><topic>Cyclin B1</topic><topic>Cytotoxicity</topic><topic>Dental Pulp - cytology</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - metabolism</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Gum disease</topic><topic>Histone deacetylase</topic><topic>Humans</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>intercellular cell adhesion molecule‐1</topic><topic>Periapical Diseases</topic><topic>Phenylbutyric acid</topic><topic>Polymerase chain reaction</topic><topic>Protein biosynthesis</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>risk factors for cardiovascular disease</topic><topic>Root canals</topic><topic>signal transduction pathways</topic><topic>Statistical analysis</topic><topic>Superoxide dismutase</topic><topic>Transcription</topic><topic>Valproic acid</topic><topic>Western blotting</topic><topic>Wound healing</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chang, Mei‐Chi</creatorcontrib><creatorcontrib>Wang, Tong‐Mei</creatorcontrib><creatorcontrib>Chien, Hua‐Hong</creatorcontrib><creatorcontrib>Pan, Yu‐Hwa</creatorcontrib><creatorcontrib>Tsai, Yi‐Ling</creatorcontrib><creatorcontrib>Jeng, Po‐Yuan</creatorcontrib><creatorcontrib>Lin, Li‐Deh</creatorcontrib><creatorcontrib>Jeng, Jiiang‐Huei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>International endodontic journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chang, Mei‐Chi</au><au>Wang, Tong‐Mei</au><au>Chien, Hua‐Hong</au><au>Pan, Yu‐Hwa</au><au>Tsai, Yi‐Ling</au><au>Jeng, Po‐Yuan</au><au>Lin, Li‐Deh</au><au>Jeng, Jiiang‐Huei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of butyrate, a bacterial by‐product, on the viability and ICAM‐1 expression/production of human vascular endothelial cells: Role in infectious pulpal/periapical diseases</atitle><jtitle>International endodontic journal</jtitle><addtitle>Int Endod J</addtitle><date>2022-01</date><risdate>2022</risdate><volume>55</volume><issue>1</issue><spage>38</spage><epage>53</epage><pages>38-53</pages><issn>0143-2885</issn><eissn>1365-2591</eissn><abstract>Aim
To investigate the effects of butyric acid (BA), a metabolic product generated by pulp and root canal pathogens, on the viability and intercellular adhesion molecule‐1 (ICAM‐1) production of endothelial cells, which are crucial to angiogenesis and pulpal/periapical wound healing.
Methodology
Endothelial cells were exposed to butyrate with/without inhibitors. Cell viability, apoptosis and reactive oxygen species (ROS) were evaluated using an MTT assay, PI/annexin V and DCF fluorescence flow cytometry respectively. RNA and protein expression was determined using a polymerase chain reaction assay and Western blotting or immunofluorescent staining. Soluble ICAM‐1 (sICAM‐1) was measured using an enzyme‐linked immunosorbent assay. The quantitative results were expressed as mean ± standard error (SE) of the mean. The data were analysed using a paired Student's t‐test where necessary. A p‐value ≤0.05 was considered to indicate a statistically significant difference between groups.
Results
Butyrate (>4 mM) inhibited cell viability and induced cellular apoptosis and necrosis. It inhibited cyclin B1 but stimulated p21 and p27 expression. Butyrate stimulated ROS production and hemeoxygenase‐1 (HO‐1) expression as well as activated the Ac‐H3, p‐ATM, p‐ATR, p‐Chk1, p‐Chk2, p‐p38 and p‐Akt expression of endothelial cells. Butyrate stimulated ICAM‐1 mRNA/protein expression and significant sICAM‐1 production (p < .05). Superoxide dismutase, 5z‐7oxozeaenol, SB203580 and compound C (p < .05), but not ZnPP, CGK733, AZD7762 or LY294002, attenuated butyrate cytotoxicity to endothelial cells. Notably, little effect on butyrate‐stimulated sICAM‐1 secretion was found. Valproic acid, phenylbutyrate and trichostatin (three histone deacetylase inhibitors) significantly induced sICAM‐1 production (p < .05).
Conclusion
Butyric acid inhibited proliferation, induced apoptosis, stimulated ROS and HO‐1 production and increased ICAM‐1 mRNA expression and protein synthesis in endothelial cells. Cell viability affected by BA was diminished by some inhibitors; however, the increased sICAM‐1 secretion by BA was not affected by any of the tested inhibitors. These results facilitate understanding of the pathogenesis, prevention and treatment of pulpal/periapical diseases.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>34420220</pmid><doi>10.1111/iej.13614</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-2068-5380</orcidid></addata></record> |
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| ispartof | International endodontic journal, 2022-01, Vol.55 (1), p.38-53 |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | AKT protein Angiogenesis Annexin V apical periodontitis Apoptosis Butyric acid Butyric Acid - pharmacology Cell adhesion Cell viability Cells, Cultured CHK1 protein Cyclin B1 Cytotoxicity Dental Pulp - cytology Endothelial cells Endothelial Cells - metabolism Flow cytometry Gene expression Gum disease Histone deacetylase Humans Intercellular Adhesion Molecule-1 - metabolism intercellular cell adhesion molecule‐1 Periapical Diseases Phenylbutyric acid Polymerase chain reaction Protein biosynthesis Protein expression Proteins Reactive oxygen species risk factors for cardiovascular disease Root canals signal transduction pathways Statistical analysis Superoxide dismutase Transcription Valproic acid Western blotting Wound healing |
| title | Effect of butyrate, a bacterial by‐product, on the viability and ICAM‐1 expression/production of human vascular endothelial cells: Role in infectious pulpal/periapical diseases |
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