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SPION primes THP1 derived M2 macrophages towards M1-like macrophages
•Monocyte differentiation alters cellular ferritin and cathepsin L levels.•Ferritin and cathepsin L are associated with plasticity in macrophages.•Iron in SPION induces a phenotypic shift in M2 macrophages.•Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes. Potentially, cellul...
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Published in: | Biochemical and biophysical research communications 2013-11, Vol.441 (4), p.737-742 |
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creator | Laskar, Amit Eilertsen, Jonas Li, Wei Yuan, Xi-Ming |
description | •Monocyte differentiation alters cellular ferritin and cathepsin L levels.•Ferritin and cathepsin L are associated with plasticity in macrophages.•Iron in SPION induces a phenotypic shift in M2 macrophages.•Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes.
Potentially, cellular iron regulates functional plasticity in macrophages yet; interaction of functionally polarized macrophages with iron-oxide nanoparticles has never been studied. We found that monocyte differentiation alters cellular ferritin and cathepsin L levels and induces functional polarization in macrophages. Iron in super paramagnetic iron-oxide nanoparticle (SPION) induces a phenotypic shift in THP1 derived M2 macrophages towards a high CD86+ and high TNF α+ macrophage subtype. This phenotypic shift was accompanied by up-regulated intracellular levels of ferritin and cathepsin L in M2 macrophages, which is a characteristic hallmark of M1 macrophages. Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes, and thus these cells may escape detection by iron-oxide nanoparticles (INPs) in-vivo. |
doi_str_mv | 10.1016/j.bbrc.2013.10.115 |
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Potentially, cellular iron regulates functional plasticity in macrophages yet; interaction of functionally polarized macrophages with iron-oxide nanoparticles has never been studied. We found that monocyte differentiation alters cellular ferritin and cathepsin L levels and induces functional polarization in macrophages. Iron in super paramagnetic iron-oxide nanoparticle (SPION) induces a phenotypic shift in THP1 derived M2 macrophages towards a high CD86+ and high TNF α+ macrophage subtype. This phenotypic shift was accompanied by up-regulated intracellular levels of ferritin and cathepsin L in M2 macrophages, which is a characteristic hallmark of M1 macrophages. Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes, and thus these cells may escape detection by iron-oxide nanoparticles (INPs) in-vivo.</description><identifier>ISSN: 0006-291X</identifier><identifier>ISSN: 1090-2104</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1016/j.bbrc.2013.10.115</identifier><identifier>PMID: 24184477</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>B7-2 Antigen - analysis ; Cathepsin L ; Cathepsin L - metabolism ; Cell Differentiation - drug effects ; Cell Polarity - drug effects ; Cells, Cultured ; Dextrans - pharmacology ; Ferric Compounds - pharmacology ; Ferritin ; Ferritins - metabolism ; Humans ; Immunoglobulin G - immunology ; Inflammation - metabolism ; Iron-oxide nanoparticles ; M1 and M2 macrophages ; Macrophages - cytology ; Macrophages - drug effects ; Macrophages - metabolism ; Magnetite Nanoparticles ; Oxysterols ; Phagocytosis - drug effects ; Plaque, Atherosclerotic - metabolism ; Sterols - pharmacology ; Tetradecanoylphorbol Acetate - analogs & derivatives ; Tetradecanoylphorbol Acetate - pharmacology ; Tumor Necrosis Factor-alpha - analysis ; Up-Regulation</subject><ispartof>Biochemical and biophysical research communications, 2013-11, Vol.441 (4), p.737-742</ispartof><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-b498b7c780a46c92cd3578aa2848e2ecf8ee5602ce67e7fee14764f26e15e6b13</citedby><cites>FETCH-LOGICAL-c393t-b498b7c780a46c92cd3578aa2848e2ecf8ee5602ce67e7fee14764f26e15e6b13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,777,781,882,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24184477$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-91999$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Laskar, Amit</creatorcontrib><creatorcontrib>Eilertsen, Jonas</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Yuan, Xi-Ming</creatorcontrib><title>SPION primes THP1 derived M2 macrophages towards M1-like macrophages</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>•Monocyte differentiation alters cellular ferritin and cathepsin L levels.•Ferritin and cathepsin L are associated with plasticity in macrophages.•Iron in SPION induces a phenotypic shift in M2 macrophages.•Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes.
Potentially, cellular iron regulates functional plasticity in macrophages yet; interaction of functionally polarized macrophages with iron-oxide nanoparticles has never been studied. We found that monocyte differentiation alters cellular ferritin and cathepsin L levels and induces functional polarization in macrophages. Iron in super paramagnetic iron-oxide nanoparticle (SPION) induces a phenotypic shift in THP1 derived M2 macrophages towards a high CD86+ and high TNF α+ macrophage subtype. This phenotypic shift was accompanied by up-regulated intracellular levels of ferritin and cathepsin L in M2 macrophages, which is a characteristic hallmark of M1 macrophages. Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes, and thus these cells may escape detection by iron-oxide nanoparticles (INPs) in-vivo.</description><subject>B7-2 Antigen - analysis</subject><subject>Cathepsin L</subject><subject>Cathepsin L - metabolism</subject><subject>Cell Differentiation - drug effects</subject><subject>Cell Polarity - drug effects</subject><subject>Cells, Cultured</subject><subject>Dextrans - pharmacology</subject><subject>Ferric Compounds - pharmacology</subject><subject>Ferritin</subject><subject>Ferritins - metabolism</subject><subject>Humans</subject><subject>Immunoglobulin G - immunology</subject><subject>Inflammation - metabolism</subject><subject>Iron-oxide nanoparticles</subject><subject>M1 and M2 macrophages</subject><subject>Macrophages - cytology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Magnetite Nanoparticles</subject><subject>Oxysterols</subject><subject>Phagocytosis - drug effects</subject><subject>Plaque, Atherosclerotic - metabolism</subject><subject>Sterols - pharmacology</subject><subject>Tetradecanoylphorbol Acetate - analogs & derivatives</subject><subject>Tetradecanoylphorbol Acetate - pharmacology</subject><subject>Tumor Necrosis Factor-alpha - analysis</subject><subject>Up-Regulation</subject><issn>0006-291X</issn><issn>1090-2104</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp9kE1PwzAMhiMEgjH4AxxQjxzoiNM0bSQu0wYMCdgkPsQtSlMXMrp1JOsm_j0tA8SJkyX78Sv7IeQIaA8oiLNpL8uc6TEKUa_tQbxFOkAlDRlQvk06lFIRMgnPe2Tf-ymlAFzIXbLHOKScJ0mHDO8n1-O7YOHsDH3wMJpAkKOzK8yDWxbMtHHV4lW_NLNltdYu98EthKV9w7-zA7JT6NLj4XftksfLi4fBKLwZX10P-jehiWS0DDMu0ywxSUo1F0Yyk0dxkmrNUp4iQ1OkiLGgzKBIMCkQgSeCF0wgxCgyiLrkdJPr17ioM9Verd2HqrRVQ_vUV5V7UaWtlQQpZYOfbPCFq95r9Es1s95gWeo5VrVXjQzOpeQpbVC2QZufvHdY_GYDVa1sNVWtbNXK_upB3Cwdf-fX2Qzz35Ufuw1wvgGwkbKy6JQ3FucGc-vQLFVe2f_yPwEfk47J</recordid><startdate>20131129</startdate><enddate>20131129</enddate><creator>Laskar, Amit</creator><creator>Eilertsen, Jonas</creator><creator>Li, Wei</creator><creator>Yuan, Xi-Ming</creator><general>Elsevier 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>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>DG8</scope></search><sort><creationdate>20131129</creationdate><title>SPION primes THP1 derived M2 macrophages towards M1-like macrophages</title><author>Laskar, Amit ; Eilertsen, Jonas ; Li, Wei ; Yuan, Xi-Ming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-b498b7c780a46c92cd3578aa2848e2ecf8ee5602ce67e7fee14764f26e15e6b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>B7-2 Antigen - analysis</topic><topic>Cathepsin L</topic><topic>Cathepsin L - metabolism</topic><topic>Cell Differentiation - drug effects</topic><topic>Cell Polarity - drug effects</topic><topic>Cells, Cultured</topic><topic>Dextrans - pharmacology</topic><topic>Ferric Compounds - pharmacology</topic><topic>Ferritin</topic><topic>Ferritins - metabolism</topic><topic>Humans</topic><topic>Immunoglobulin G - immunology</topic><topic>Inflammation - metabolism</topic><topic>Iron-oxide nanoparticles</topic><topic>M1 and M2 macrophages</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Magnetite Nanoparticles</topic><topic>Oxysterols</topic><topic>Phagocytosis - drug effects</topic><topic>Plaque, Atherosclerotic - metabolism</topic><topic>Sterols - pharmacology</topic><topic>Tetradecanoylphorbol Acetate - analogs & derivatives</topic><topic>Tetradecanoylphorbol Acetate - pharmacology</topic><topic>Tumor Necrosis Factor-alpha - analysis</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Laskar, Amit</creatorcontrib><creatorcontrib>Eilertsen, Jonas</creatorcontrib><creatorcontrib>Li, Wei</creatorcontrib><creatorcontrib>Yuan, Xi-Ming</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>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Linköpings universitet</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Laskar, Amit</au><au>Eilertsen, Jonas</au><au>Li, Wei</au><au>Yuan, Xi-Ming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SPION primes THP1 derived M2 macrophages towards M1-like macrophages</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>2013-11-29</date><risdate>2013</risdate><volume>441</volume><issue>4</issue><spage>737</spage><epage>742</epage><pages>737-742</pages><issn>0006-291X</issn><issn>1090-2104</issn><eissn>1090-2104</eissn><abstract>•Monocyte differentiation alters cellular ferritin and cathepsin L levels.•Ferritin and cathepsin L are associated with plasticity in macrophages.•Iron in SPION induces a phenotypic shift in M2 macrophages.•Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes.
Potentially, cellular iron regulates functional plasticity in macrophages yet; interaction of functionally polarized macrophages with iron-oxide nanoparticles has never been studied. We found that monocyte differentiation alters cellular ferritin and cathepsin L levels and induces functional polarization in macrophages. Iron in super paramagnetic iron-oxide nanoparticle (SPION) induces a phenotypic shift in THP1 derived M2 macrophages towards a high CD86+ and high TNF α+ macrophage subtype. This phenotypic shift was accompanied by up-regulated intracellular levels of ferritin and cathepsin L in M2 macrophages, which is a characteristic hallmark of M1 macrophages. Atherogenic oxysterols reduce phagocytic activity in macrophage subtypes, and thus these cells may escape detection by iron-oxide nanoparticles (INPs) in-vivo.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>24184477</pmid><doi>10.1016/j.bbrc.2013.10.115</doi><tpages>6</tpages></addata></record> |
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subjects | B7-2 Antigen - analysis Cathepsin L Cathepsin L - metabolism Cell Differentiation - drug effects Cell Polarity - drug effects Cells, Cultured Dextrans - pharmacology Ferric Compounds - pharmacology Ferritin Ferritins - metabolism Humans Immunoglobulin G - immunology Inflammation - metabolism Iron-oxide nanoparticles M1 and M2 macrophages Macrophages - cytology Macrophages - drug effects Macrophages - metabolism Magnetite Nanoparticles Oxysterols Phagocytosis - drug effects Plaque, Atherosclerotic - metabolism Sterols - pharmacology Tetradecanoylphorbol Acetate - analogs & derivatives Tetradecanoylphorbol Acetate - pharmacology Tumor Necrosis Factor-alpha - analysis Up-Regulation |
title | SPION primes THP1 derived M2 macrophages towards M1-like macrophages |
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