Olive phenols preserve lamin B1 expression reducing cGAS/STING/NFκB‐mediated SASP in ionizing radiation‐induced senescence
Senescence occurs upon critical telomere shortening, or following DNA damage, oncogenic activation, hypoxia and oxidative stress, overall referred to stress‐induced premature senescence (SIPS). In response to DNA damage, senescent cells release cytoplasmic chromatin fragments (CCFs), and express an...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2022-04, Vol.26 (8), p.2337-2350 |
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| creator | Frediani, Elena Scavone, Francesca Laurenzana, Anna Chillà, Anastasia Tortora, Katia Cimmino, Ilaria Leri, Manuela Bucciantini, Monica Mangoni, Monica Fibbi, Gabriella Del Rosso, Mario Mocali, Alessandra Giovannelli, Lisa Margheri, Francesca |
| description | Senescence occurs upon critical telomere shortening, or following DNA damage, oncogenic activation, hypoxia and oxidative stress, overall referred to stress‐induced premature senescence (SIPS). In response to DNA damage, senescent cells release cytoplasmic chromatin fragments (CCFs), and express an altered secretome, the senescence‐associated secretory phenotype (SASP), which contributes to generate a pro‐inflammatory and pro‐tumoral extracellular milieu. Polyphenols have gained significant attention owing to their anti‐inflammatory and anti‐tumour activities. Here, we studied the effect of oleuropein aglycone (OLE) and hydroxytyrosol (HT) on DNA damage, CCF appearance and SASP in a model of irradiation‐induced senescence. Neonatal human dermal fibroblasts (NHDFs) were γ‐irradiated and incubated with OLE, 5 µM and HT, 1 µM. Cell growth and senescence‐associated (SA)‐β‐Gal‐staining were used as senescence markers. DNA damage was evaluated by Comet assay, lamin B1 expression, release of CCFs, cyclic GMP‐AMP Synthase (cGAS) activation. IL‐6, IL‐8, MCP‐1 and RANTES were measured by ELISA assay. Our results showed that OLE and HT exerted a protective effect on 8 Gy irradiation‐induced senescence, preserving lamin B1 expression and reducing cGAS/STING/NFκB‐mediated SASP. The ability of OLE and HT to mitigate DNA damage, senescence status and the related SASP in normal cells can be exploited to improve the efficacy and safety of cancer radiotherapy. |
| doi_str_mv | 10.1111/jcmm.17255 |
| format | Article |
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In response to DNA damage, senescent cells release cytoplasmic chromatin fragments (CCFs), and express an altered secretome, the senescence‐associated secretory phenotype (SASP), which contributes to generate a pro‐inflammatory and pro‐tumoral extracellular milieu. Polyphenols have gained significant attention owing to their anti‐inflammatory and anti‐tumour activities. Here, we studied the effect of oleuropein aglycone (OLE) and hydroxytyrosol (HT) on DNA damage, CCF appearance and SASP in a model of irradiation‐induced senescence. Neonatal human dermal fibroblasts (NHDFs) were γ‐irradiated and incubated with OLE, 5 µM and HT, 1 µM. Cell growth and senescence‐associated (SA)‐β‐Gal‐staining were used as senescence markers. DNA damage was evaluated by Comet assay, lamin B1 expression, release of CCFs, cyclic GMP‐AMP Synthase (cGAS) activation. IL‐6, IL‐8, MCP‐1 and RANTES were measured by ELISA assay. Our results showed that OLE and HT exerted a protective effect on 8 Gy irradiation‐induced senescence, preserving lamin B1 expression and reducing cGAS/STING/NFκB‐mediated SASP. The ability of OLE and HT to mitigate DNA damage, senescence status and the related SASP in normal cells can be exploited to improve the efficacy and safety of cancer radiotherapy.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.17255</identifier><identifier>PMID: 35278036</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Antibodies ; Cell culture ; Cell cycle ; Cellular Senescence ; Chromatin ; Comet assay ; Cyclic GMP ; Deoxyribonucleic acid ; DNA ; DNA Damage ; Enzyme-linked immunosorbent assay ; Fibroblasts ; human fibroblasts ; Humans ; Hypoxia ; Inflammation ; Interleukin 6 ; Ionizing radiation ; Lamin Type B ; Morphology ; Neonates ; Neoplasms - metabolism ; NF-kappa B - genetics ; NF-κB protein ; Nucleotidyltransferases - genetics ; Olea - metabolism ; Original ; Oxidative stress ; Phenols ; Phenols - pharmacology ; Phenotypes ; Polyphenols ; Radiation ; Radiation therapy ; Radiation, Ionizing ; radiation‐induced senescence ; RANTES ; SASP ; Secretome ; Senescence ; Telomeres ; Tumors</subject><ispartof>Journal of cellular and molecular medicine, 2022-04, Vol.26 (8), p.2337-2350</ispartof><rights>2022 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022. This work is published 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.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4485-e9ee2b66c651b7a5de1d9330a0a7f4db1221ec44901b61c72aaf74b3469bb1b23</citedby><cites>FETCH-LOGICAL-c4485-e9ee2b66c651b7a5de1d9330a0a7f4db1221ec44901b61c72aaf74b3469bb1b23</cites><orcidid>0000-0001-7122-6574</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8995441/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8995441/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35278036$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Frediani, Elena</creatorcontrib><creatorcontrib>Scavone, Francesca</creatorcontrib><creatorcontrib>Laurenzana, Anna</creatorcontrib><creatorcontrib>Chillà, Anastasia</creatorcontrib><creatorcontrib>Tortora, Katia</creatorcontrib><creatorcontrib>Cimmino, Ilaria</creatorcontrib><creatorcontrib>Leri, Manuela</creatorcontrib><creatorcontrib>Bucciantini, Monica</creatorcontrib><creatorcontrib>Mangoni, Monica</creatorcontrib><creatorcontrib>Fibbi, Gabriella</creatorcontrib><creatorcontrib>Del Rosso, Mario</creatorcontrib><creatorcontrib>Mocali, Alessandra</creatorcontrib><creatorcontrib>Giovannelli, Lisa</creatorcontrib><creatorcontrib>Margheri, Francesca</creatorcontrib><title>Olive phenols preserve lamin B1 expression reducing cGAS/STING/NFκB‐mediated SASP in ionizing radiation‐induced senescence</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Senescence occurs upon critical telomere shortening, or following DNA damage, oncogenic activation, hypoxia and oxidative stress, overall referred to stress‐induced premature senescence (SIPS). In response to DNA damage, senescent cells release cytoplasmic chromatin fragments (CCFs), and express an altered secretome, the senescence‐associated secretory phenotype (SASP), which contributes to generate a pro‐inflammatory and pro‐tumoral extracellular milieu. Polyphenols have gained significant attention owing to their anti‐inflammatory and anti‐tumour activities. Here, we studied the effect of oleuropein aglycone (OLE) and hydroxytyrosol (HT) on DNA damage, CCF appearance and SASP in a model of irradiation‐induced senescence. Neonatal human dermal fibroblasts (NHDFs) were γ‐irradiated and incubated with OLE, 5 µM and HT, 1 µM. Cell growth and senescence‐associated (SA)‐β‐Gal‐staining were used as senescence markers. DNA damage was evaluated by Comet assay, lamin B1 expression, release of CCFs, cyclic GMP‐AMP Synthase (cGAS) activation. IL‐6, IL‐8, MCP‐1 and RANTES were measured by ELISA assay. Our results showed that OLE and HT exerted a protective effect on 8 Gy irradiation‐induced senescence, preserving lamin B1 expression and reducing cGAS/STING/NFκB‐mediated SASP. The ability of OLE and HT to mitigate DNA damage, senescence status and the related SASP in normal cells can be exploited to improve the efficacy and safety of cancer radiotherapy.</description><subject>Antibodies</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cellular Senescence</subject><subject>Chromatin</subject><subject>Comet assay</subject><subject>Cyclic GMP</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA Damage</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Fibroblasts</subject><subject>human fibroblasts</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Inflammation</subject><subject>Interleukin 6</subject><subject>Ionizing radiation</subject><subject>Lamin Type B</subject><subject>Morphology</subject><subject>Neonates</subject><subject>Neoplasms - metabolism</subject><subject>NF-kappa B - genetics</subject><subject>NF-κB protein</subject><subject>Nucleotidyltransferases - genetics</subject><subject>Olea - metabolism</subject><subject>Original</subject><subject>Oxidative stress</subject><subject>Phenols</subject><subject>Phenols - pharmacology</subject><subject>Phenotypes</subject><subject>Polyphenols</subject><subject>Radiation</subject><subject>Radiation therapy</subject><subject>Radiation, Ionizing</subject><subject>radiation‐induced senescence</subject><subject>RANTES</subject><subject>SASP</subject><subject>Secretome</subject><subject>Senescence</subject><subject>Telomeres</subject><subject>Tumors</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1uEzEQxy0EoiVw4QHQSlwQUpr1x-7aF6Q0oqGoH0gpZ8v2TlpHu97UzhbKBR6B5-EheAiehFkSKuCAL_aMf_P3jP-EPKX5AcU1Wbm2PaAVK4p7ZJ8Wko2F4uL-7kwll3vkUUqrPOcl5eoh2eMFqyRG--TzeeNvIFtfQeialK0jJIiYaEzrQ3ZIM_g45JLvQhah7p0Pl5mbTxeTxcXx2XxydvT92-GPL19bqL3ZQJ0tpot3GZZigf80wNEMNxgi5QMqIJQgQHIQHDwmD5amSfBkt4_I-6PXF7M345Pz-fFsejJ2QshiDAqA2bJ0ZUFtZYoaaK04z01uqqWoLWWMAqIqp7akrmLGLCthuSiVtdQyPiKvtrrr3mKv-PYmmkavo29NvNWd8frvm-Cv9GV3o6VShRAUBV7sBGJ33UPa6NbjCE1jAnR90qzkshIyx08ekef_oKuujwHHQ0pISQvGFVIvt5SLXUoRlnfN0FwPvurBV_3LV4Sf_dn-HfrbSAToFvjgG7j9j5R-Ozs93Yr-BFmosck</recordid><startdate>202204</startdate><enddate>202204</enddate><creator>Frediani, Elena</creator><creator>Scavone, Francesca</creator><creator>Laurenzana, Anna</creator><creator>Chillà, Anastasia</creator><creator>Tortora, Katia</creator><creator>Cimmino, Ilaria</creator><creator>Leri, Manuela</creator><creator>Bucciantini, Monica</creator><creator>Mangoni, Monica</creator><creator>Fibbi, Gabriella</creator><creator>Del Rosso, Mario</creator><creator>Mocali, Alessandra</creator><creator>Giovannelli, Lisa</creator><creator>Margheri, Francesca</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7122-6574</orcidid></search><sort><creationdate>202204</creationdate><title>Olive phenols preserve lamin B1 expression reducing cGAS/STING/NFκB‐mediated SASP in ionizing radiation‐induced senescence</title><author>Frediani, Elena ; Scavone, Francesca ; Laurenzana, Anna ; Chillà, Anastasia ; Tortora, Katia ; Cimmino, Ilaria ; Leri, Manuela ; Bucciantini, Monica ; Mangoni, Monica ; Fibbi, Gabriella ; Del Rosso, Mario ; Mocali, Alessandra ; Giovannelli, Lisa ; Margheri, Francesca</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4485-e9ee2b66c651b7a5de1d9330a0a7f4db1221ec44901b61c72aaf74b3469bb1b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Antibodies</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cellular Senescence</topic><topic>Chromatin</topic><topic>Comet assay</topic><topic>Cyclic GMP</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>DNA Damage</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Fibroblasts</topic><topic>human fibroblasts</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Inflammation</topic><topic>Interleukin 6</topic><topic>Ionizing radiation</topic><topic>Lamin Type B</topic><topic>Morphology</topic><topic>Neonates</topic><topic>Neoplasms - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Frediani, Elena</au><au>Scavone, Francesca</au><au>Laurenzana, Anna</au><au>Chillà, Anastasia</au><au>Tortora, Katia</au><au>Cimmino, Ilaria</au><au>Leri, Manuela</au><au>Bucciantini, Monica</au><au>Mangoni, Monica</au><au>Fibbi, Gabriella</au><au>Del Rosso, Mario</au><au>Mocali, Alessandra</au><au>Giovannelli, Lisa</au><au>Margheri, Francesca</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Olive phenols preserve lamin B1 expression reducing cGAS/STING/NFκB‐mediated SASP in ionizing radiation‐induced senescence</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2022-04</date><risdate>2022</risdate><volume>26</volume><issue>8</issue><spage>2337</spage><epage>2350</epage><pages>2337-2350</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Senescence occurs upon critical telomere shortening, or following DNA damage, oncogenic activation, hypoxia and oxidative stress, overall referred to stress‐induced premature senescence (SIPS). In response to DNA damage, senescent cells release cytoplasmic chromatin fragments (CCFs), and express an altered secretome, the senescence‐associated secretory phenotype (SASP), which contributes to generate a pro‐inflammatory and pro‐tumoral extracellular milieu. Polyphenols have gained significant attention owing to their anti‐inflammatory and anti‐tumour activities. Here, we studied the effect of oleuropein aglycone (OLE) and hydroxytyrosol (HT) on DNA damage, CCF appearance and SASP in a model of irradiation‐induced senescence. Neonatal human dermal fibroblasts (NHDFs) were γ‐irradiated and incubated with OLE, 5 µM and HT, 1 µM. Cell growth and senescence‐associated (SA)‐β‐Gal‐staining were used as senescence markers. DNA damage was evaluated by Comet assay, lamin B1 expression, release of CCFs, cyclic GMP‐AMP Synthase (cGAS) activation. IL‐6, IL‐8, MCP‐1 and RANTES were measured by ELISA assay. Our results showed that OLE and HT exerted a protective effect on 8 Gy irradiation‐induced senescence, preserving lamin B1 expression and reducing cGAS/STING/NFκB‐mediated SASP. The ability of OLE and HT to mitigate DNA damage, senescence status and the related SASP in normal cells can be exploited to improve the efficacy and safety of cancer radiotherapy.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>35278036</pmid><doi>10.1111/jcmm.17255</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-7122-6574</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Journals; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Wiley-Blackwell Open Access Titles; PubMed Central |
| subjects | Antibodies Cell culture Cell cycle Cellular Senescence Chromatin Comet assay Cyclic GMP Deoxyribonucleic acid DNA DNA Damage Enzyme-linked immunosorbent assay Fibroblasts human fibroblasts Humans Hypoxia Inflammation Interleukin 6 Ionizing radiation Lamin Type B Morphology Neonates Neoplasms - metabolism NF-kappa B - genetics NF-κB protein Nucleotidyltransferases - genetics Olea - metabolism Original Oxidative stress Phenols Phenols - pharmacology Phenotypes Polyphenols Radiation Radiation therapy Radiation, Ionizing radiation‐induced senescence RANTES SASP Secretome Senescence Telomeres Tumors |
| title | Olive phenols preserve lamin B1 expression reducing cGAS/STING/NFκB‐mediated SASP in ionizing radiation‐induced senescence |
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