Activation of autophagy in macrophages by pro-resolving lipid mediators
The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA 4 and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic infla...
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| Veröffentlicht in: | Autophagy 2015-10, Vol.11 (10), p.1729-1744 |
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| creator | Prieto, Patricia Rosales-Mendoza, César Eduardo Terrón, Verónica Toledano, Víctor Cuadrado, Antonio López-Collazo, Eduardo Bannenberg, Gerard Martín-Sanz, Paloma Fernández-Velasco, María Boscá, Lisardo |
| description | The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA
4
and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA
4
and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3
+
autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA
4
and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA
4
and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases. |
| doi_str_mv | 10.1080/15548627.2015.1078958 |
| format | Article |
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4
and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA
4
and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3
+
autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA
4
and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA
4
and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.</description><identifier>ISSN: 1554-8627</identifier><identifier>ISSN: 1554-8635</identifier><identifier>EISSN: 1554-8635</identifier><identifier>DOI: 10.1080/15548627.2015.1078958</identifier><identifier>PMID: 26506892</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>15-epi-lipoxin-A ; Animals ; Apoptosis - physiology ; Autophagy - genetics ; Autophagy - physiology ; Basic Research Papers ; Cytokines - metabolism ; Docosahexaenoic Acids - metabolism ; Half-Life ; inflammation ; Inflammation - metabolism ; Lipoxins - metabolism ; Macrophages - cytology ; macrophages resolution ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; resolvin-D1</subject><ispartof>Autophagy, 2015-10, Vol.11 (10), p.1729-1744</ispartof><rights>2015 Taylor & Francis Group, LLC 2015</rights><rights>2015 Taylor & Francis Group, LLC 2015 Taylor & Francis Group, LLC</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c534t-aee34bc0cc1e8be63af3906d1ccffb77e0a16b22f4dbe68586e2007aca3390573</citedby><cites>FETCH-LOGICAL-c534t-aee34bc0cc1e8be63af3906d1ccffb77e0a16b22f4dbe68586e2007aca3390573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4824594/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4824594/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26506892$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Prieto, Patricia</creatorcontrib><creatorcontrib>Rosales-Mendoza, César Eduardo</creatorcontrib><creatorcontrib>Terrón, Verónica</creatorcontrib><creatorcontrib>Toledano, Víctor</creatorcontrib><creatorcontrib>Cuadrado, Antonio</creatorcontrib><creatorcontrib>López-Collazo, Eduardo</creatorcontrib><creatorcontrib>Bannenberg, Gerard</creatorcontrib><creatorcontrib>Martín-Sanz, Paloma</creatorcontrib><creatorcontrib>Fernández-Velasco, María</creatorcontrib><creatorcontrib>Boscá, Lisardo</creatorcontrib><title>Activation of autophagy in macrophages by pro-resolving lipid mediators</title><title>Autophagy</title><addtitle>Autophagy</addtitle><description>The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA
4
and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA
4
and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3
+
autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA
4
and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA
4
and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.</description><subject>15-epi-lipoxin-A</subject><subject>Animals</subject><subject>Apoptosis - physiology</subject><subject>Autophagy - genetics</subject><subject>Autophagy - physiology</subject><subject>Basic Research Papers</subject><subject>Cytokines - metabolism</subject><subject>Docosahexaenoic Acids - metabolism</subject><subject>Half-Life</subject><subject>inflammation</subject><subject>Inflammation - metabolism</subject><subject>Lipoxins - metabolism</subject><subject>Macrophages - cytology</subject><subject>macrophages resolution</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>resolvin-D1</subject><issn>1554-8627</issn><issn>1554-8635</issn><issn>1554-8635</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UctOwzAQtBAIyuMTQDlyCfgRx-4FgSooSJW4wNnaOHYxSuJgp0X9e1xaKrhw2tfszGoHoXOCrwiW-JpwXsiSiiuKCU8tIcdc7qHRup_LkvH9XU7FETqO8R1jVsoxPURHtOR4nY7Q9E4PbgmD813mbQaLwfdvMF9lrsta0OG7MjGrVlkffB5M9M3SdfOscb2rs9bUDgYf4ik6sNBEc7aNJ-j14f5l8pjPnqdPk7tZrjkrhhyMYUWlsdbEyMqUDCwb47ImWltbCWEwkLKi1BZ1mkouS0MxFqCBJRwX7ATdbHj7RZXEtemGAI3qg2shrJQHp_5OOvem5n6pCkkLPi4SweWWIPiPhYmDal3UpmmgM34RFRFUUi4IwQnKN9D0hhiDsTsZgtXaBPVjglqboLYmpL2L3zfutn6-ngC3G4DrrA8tfPrQ1GqAVeODDdBpFxX7X-MLCpeY6w</recordid><startdate>20151003</startdate><enddate>20151003</enddate><creator>Prieto, Patricia</creator><creator>Rosales-Mendoza, César Eduardo</creator><creator>Terrón, Verónica</creator><creator>Toledano, Víctor</creator><creator>Cuadrado, Antonio</creator><creator>López-Collazo, Eduardo</creator><creator>Bannenberg, Gerard</creator><creator>Martín-Sanz, Paloma</creator><creator>Fernández-Velasco, María</creator><creator>Boscá, Lisardo</creator><general>Taylor & Francis</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20151003</creationdate><title>Activation of autophagy in macrophages by pro-resolving lipid mediators</title><author>Prieto, Patricia ; Rosales-Mendoza, César Eduardo ; Terrón, Verónica ; Toledano, Víctor ; Cuadrado, Antonio ; López-Collazo, Eduardo ; Bannenberg, Gerard ; Martín-Sanz, Paloma ; Fernández-Velasco, María ; Boscá, Lisardo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c534t-aee34bc0cc1e8be63af3906d1ccffb77e0a16b22f4dbe68586e2007aca3390573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>15-epi-lipoxin-A</topic><topic>Animals</topic><topic>Apoptosis - physiology</topic><topic>Autophagy - genetics</topic><topic>Autophagy - physiology</topic><topic>Basic Research Papers</topic><topic>Cytokines - metabolism</topic><topic>Docosahexaenoic Acids - metabolism</topic><topic>Half-Life</topic><topic>inflammation</topic><topic>Inflammation - metabolism</topic><topic>Lipoxins - metabolism</topic><topic>Macrophages - cytology</topic><topic>macrophages resolution</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>resolvin-D1</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Prieto, Patricia</creatorcontrib><creatorcontrib>Rosales-Mendoza, César Eduardo</creatorcontrib><creatorcontrib>Terrón, Verónica</creatorcontrib><creatorcontrib>Toledano, Víctor</creatorcontrib><creatorcontrib>Cuadrado, Antonio</creatorcontrib><creatorcontrib>López-Collazo, Eduardo</creatorcontrib><creatorcontrib>Bannenberg, Gerard</creatorcontrib><creatorcontrib>Martín-Sanz, Paloma</creatorcontrib><creatorcontrib>Fernández-Velasco, María</creatorcontrib><creatorcontrib>Boscá, Lisardo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Autophagy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Prieto, Patricia</au><au>Rosales-Mendoza, César Eduardo</au><au>Terrón, Verónica</au><au>Toledano, Víctor</au><au>Cuadrado, Antonio</au><au>López-Collazo, Eduardo</au><au>Bannenberg, Gerard</au><au>Martín-Sanz, Paloma</au><au>Fernández-Velasco, María</au><au>Boscá, Lisardo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Activation of autophagy in macrophages by pro-resolving lipid mediators</atitle><jtitle>Autophagy</jtitle><addtitle>Autophagy</addtitle><date>2015-10-03</date><risdate>2015</risdate><volume>11</volume><issue>10</issue><spage>1729</spage><epage>1744</epage><pages>1729-1744</pages><issn>1554-8627</issn><issn>1554-8635</issn><eissn>1554-8635</eissn><abstract>The resolution of inflammation is an active process driven by specialized pro-resolving lipid mediators, such as 15-epi-LXA
4
and resolvin D1 (RvD1), that promote tissue regeneration. Macrophages regulate the innate immune response being key players during the resolution phase to avoid chronic inflammatory pathologies. Their half-life is tightly regulated to accomplish its phagocytic function, allowing the complete cleaning of the affected area. The balance between apoptosis and autophagy appears to be essential to control the survival of these immune cells within the inflammatory context. In the present work, we demonstrate that 15-epi-LXA
4
and RvD1 at nanomolar concentrations promote autophagy in murine and human macrophages. Both compounds induced the MAP1LC3-I to MAP1LC3-II processing and the degradation of SQSTM1 as well as the formation of MAP1LC3
+
autophagosomes, a typical signature of autophagy. Furthermore, 15-epi-LXA
4
and RvD1 treatment favored the fusion of the autophagosomes with lysosomes, allowing the final processing of the autophagic vesicles. This autophagic response involves the activation of MAPK1 and NFE2L2 pathways, but by an MTOR-independent mechanism. Moreover, these pro-resolving lipids improved the phagocytic activity of macrophages via NFE2L2. Therefore, 15-epi-LXA
4
and RvD1 improved both survival and functionality of macrophages, which likely supports the recovery of tissue homeostasis and avoiding chronic inflammatory diseases.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>26506892</pmid><doi>10.1080/15548627.2015.1078958</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | 15-epi-lipoxin-A Animals Apoptosis - physiology Autophagy - genetics Autophagy - physiology Basic Research Papers Cytokines - metabolism Docosahexaenoic Acids - metabolism Half-Life inflammation Inflammation - metabolism Lipoxins - metabolism Macrophages - cytology macrophages resolution Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout resolvin-D1 |
| title | Activation of autophagy in macrophages by pro-resolving lipid mediators |
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