15-Deoxy-Δ 12,14 -Prostaglandin J 2 Exerts Proresolving Effects Through Nuclear Factor E2-Related Factor 2-Induced Expression of CD36 and Heme Oxygenase-1
15-Deoxy-Δ -prostaglandin J (15d-PGJ ) has been shown to rescue cells from inflammatory insults and to participate in the resolution of acute inflammation. In this study, we investigated molecular mechanisms underlying proresolving effects of 15d-PGJ . 15d-PGJ injected into the peritoneum of mice fa...
Gespeichert in:
| Veröffentlicht in: | Antioxidants & redox signaling 2017-12, Vol.27 (17), p.1412-1431 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1431 |
|---|---|
| container_issue | 17 |
| container_start_page | 1412 |
| container_title | Antioxidants & redox signaling |
| container_volume | 27 |
| creator | Kim, Wonki Lee, Ha-Na Jang, Jeong-Hoon Kim, Seung Hyeon Lee, Yeon-Hwa Hahn, Young-Il Ngo, Hoang-Kieu-Chi Choi, Yeonseo Joe, Yeonsoo Chung, Hun Taeg Chen, Yingqing Cha, Young Nam Surh, Young-Joon |
| description | 15-Deoxy-Δ
-prostaglandin J
(15d-PGJ
) has been shown to rescue cells from inflammatory insults and to participate in the resolution of acute inflammation. In this study, we investigated molecular mechanisms underlying proresolving effects of 15d-PGJ
.
15d-PGJ
injected into the peritoneum of mice facilitated the resolution of zymosan A-induced peritonitis. 15d-PGJ
administration reduced the number of total leukocytes and attenuated polymorphonuclear leukocyte infiltration. Furthermore, 15d-PGJ
increased the proportion of macrophages engulfing apoptotic neutrophils, a process called efferocytosis. In addition, when the thioglycollate-elicited mouse peritoneal macrophages were stimulated with 15d-PGJ
, their efferocytic activity was amplified. In another experiment, RAW264.7 murine macrophages exposed to 15d-PGJ
conducted phagocytic clearance of apoptotic cells to a greater extent than the control cells. Under these conditions, expression of CD36 and heme oxygenase-1 (HO-1) was enhanced along with increased accumulation of the nuclear factor E2-related factor 2 (Nrf2) in the nucleus. Knockdown of Nrf2 abolished 15d-PGJ
-induced expression of CD36 and HO-1, and silencing of CD36 and HO-1 attenuated 15d-PGJ
-induced efferocytosis. Moreover, peritoneal macrophages isolated from Nrf2-null mice failed to upregulate 15d-PGJ
-induced expression of CD36 and HO-1 and to mediate efferocytosis. Unlike 15d-PGJ
, its nonelectrophilic analog 9,10-dihydro-15d-PGJ
lacking the α,β-unsaturated carbonyl group could not induce CD36 expression and efferocytosis.
15d-PGJ
, as one of the terminal products of cyclooxygenase-2, exerts proresolving effects through induction of efferocytosis. The results of this study suggest that 15d-PGJ
possesses a therapeutic value in the management of inflammatory disorders.
15d-PGJ
facilitates resolution of inflammation by inducing Nrf2-induced expression of CD36 and HO-1 in macrophages. Antioxid. Redox Signal. 27, 1412-1431. |
| doi_str_mv | 10.1089/ars.2016.6754 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1089_ars_2016_6754</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>28398824</sourcerecordid><originalsourceid>FETCH-LOGICAL-c1054-55fec20d66bdc69879afe53537ebf39fa173deab5f6d017b08e857fb2abc994b3</originalsourceid><addsrcrecordid>eNo9kM9OwkAQxjdGI4gevZp9ABf3T3e3PRoogiFiDJ6bbTsLmNKSXWrgPbz5Tj6TSxBPM_nmyzczP4RuGe0zGicPxvk-p0z1lZbRGeoyKTXRmqnzQ88FobGKOujK-w9KKWeMXqIOj0USxzzqom8myRCa3Z78fGHG71mEyatr_NYsKlOXqxo_Y47THbitx2HgwDfV56pe4NRaKII4X7qmXSzxS1tUYBwemWLbOJxy8gaV2UJ5UjiZ1GVbBCHdbUKOXzU1biweDIXCYRcewxrwbLdfQG08EHaNLqypPNz81R56H6XzwZhMZ0-TweOUFIzKiEgZDuG0VCovC5XEOjEWpJBCQ25FYg3TogSTS6tKynROY4iltjk3eZEkUS56iBxzi_C4d2CzjVutjdtnjGYHyFmAnB0gZwfIwX939G_afA3lv_tEVfwCrLx4JA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>15-Deoxy-Δ 12,14 -Prostaglandin J 2 Exerts Proresolving Effects Through Nuclear Factor E2-Related Factor 2-Induced Expression of CD36 and Heme Oxygenase-1</title><source>MEDLINE</source><source>Alma/SFX Local Collection</source><creator>Kim, Wonki ; Lee, Ha-Na ; Jang, Jeong-Hoon ; Kim, Seung Hyeon ; Lee, Yeon-Hwa ; Hahn, Young-Il ; Ngo, Hoang-Kieu-Chi ; Choi, Yeonseo ; Joe, Yeonsoo ; Chung, Hun Taeg ; Chen, Yingqing ; Cha, Young Nam ; Surh, Young-Joon</creator><creatorcontrib>Kim, Wonki ; Lee, Ha-Na ; Jang, Jeong-Hoon ; Kim, Seung Hyeon ; Lee, Yeon-Hwa ; Hahn, Young-Il ; Ngo, Hoang-Kieu-Chi ; Choi, Yeonseo ; Joe, Yeonsoo ; Chung, Hun Taeg ; Chen, Yingqing ; Cha, Young Nam ; Surh, Young-Joon</creatorcontrib><description>15-Deoxy-Δ
-prostaglandin J
(15d-PGJ
) has been shown to rescue cells from inflammatory insults and to participate in the resolution of acute inflammation. In this study, we investigated molecular mechanisms underlying proresolving effects of 15d-PGJ
.
15d-PGJ
injected into the peritoneum of mice facilitated the resolution of zymosan A-induced peritonitis. 15d-PGJ
administration reduced the number of total leukocytes and attenuated polymorphonuclear leukocyte infiltration. Furthermore, 15d-PGJ
increased the proportion of macrophages engulfing apoptotic neutrophils, a process called efferocytosis. In addition, when the thioglycollate-elicited mouse peritoneal macrophages were stimulated with 15d-PGJ
, their efferocytic activity was amplified. In another experiment, RAW264.7 murine macrophages exposed to 15d-PGJ
conducted phagocytic clearance of apoptotic cells to a greater extent than the control cells. Under these conditions, expression of CD36 and heme oxygenase-1 (HO-1) was enhanced along with increased accumulation of the nuclear factor E2-related factor 2 (Nrf2) in the nucleus. Knockdown of Nrf2 abolished 15d-PGJ
-induced expression of CD36 and HO-1, and silencing of CD36 and HO-1 attenuated 15d-PGJ
-induced efferocytosis. Moreover, peritoneal macrophages isolated from Nrf2-null mice failed to upregulate 15d-PGJ
-induced expression of CD36 and HO-1 and to mediate efferocytosis. Unlike 15d-PGJ
, its nonelectrophilic analog 9,10-dihydro-15d-PGJ
lacking the α,β-unsaturated carbonyl group could not induce CD36 expression and efferocytosis.
15d-PGJ
, as one of the terminal products of cyclooxygenase-2, exerts proresolving effects through induction of efferocytosis. The results of this study suggest that 15d-PGJ
possesses a therapeutic value in the management of inflammatory disorders.
15d-PGJ
facilitates resolution of inflammation by inducing Nrf2-induced expression of CD36 and HO-1 in macrophages. Antioxid. Redox Signal. 27, 1412-1431.</description><identifier>ISSN: 1523-0864</identifier><identifier>EISSN: 1557-7716</identifier><identifier>DOI: 10.1089/ars.2016.6754</identifier><identifier>PMID: 28398824</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; CD36 Antigens - metabolism ; Gene Expression Regulation - drug effects ; Heme Oxygenase-1 - metabolism ; Humans ; Jurkat Cells ; Macrophages - cytology ; Macrophages - drug effects ; Macrophages - metabolism ; Mice ; NF-E2-Related Factor 2 - metabolism ; Peritonitis - chemically induced ; Peritonitis - drug therapy ; Phagocytosis ; Prostaglandin D2 - administration & dosage ; Prostaglandin D2 - analogs & derivatives ; Prostaglandin D2 - pharmacology ; RAW 264.7 Cells ; Zymosan - adverse effects</subject><ispartof>Antioxidants & redox signaling, 2017-12, Vol.27 (17), p.1412-1431</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c1054-55fec20d66bdc69879afe53537ebf39fa173deab5f6d017b08e857fb2abc994b3</citedby><cites>FETCH-LOGICAL-c1054-55fec20d66bdc69879afe53537ebf39fa173deab5f6d017b08e857fb2abc994b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28398824$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Wonki</creatorcontrib><creatorcontrib>Lee, Ha-Na</creatorcontrib><creatorcontrib>Jang, Jeong-Hoon</creatorcontrib><creatorcontrib>Kim, Seung Hyeon</creatorcontrib><creatorcontrib>Lee, Yeon-Hwa</creatorcontrib><creatorcontrib>Hahn, Young-Il</creatorcontrib><creatorcontrib>Ngo, Hoang-Kieu-Chi</creatorcontrib><creatorcontrib>Choi, Yeonseo</creatorcontrib><creatorcontrib>Joe, Yeonsoo</creatorcontrib><creatorcontrib>Chung, Hun Taeg</creatorcontrib><creatorcontrib>Chen, Yingqing</creatorcontrib><creatorcontrib>Cha, Young Nam</creatorcontrib><creatorcontrib>Surh, Young-Joon</creatorcontrib><title>15-Deoxy-Δ 12,14 -Prostaglandin J 2 Exerts Proresolving Effects Through Nuclear Factor E2-Related Factor 2-Induced Expression of CD36 and Heme Oxygenase-1</title><title>Antioxidants & redox signaling</title><addtitle>Antioxid Redox Signal</addtitle><description>15-Deoxy-Δ
-prostaglandin J
(15d-PGJ
) has been shown to rescue cells from inflammatory insults and to participate in the resolution of acute inflammation. In this study, we investigated molecular mechanisms underlying proresolving effects of 15d-PGJ
.
15d-PGJ
injected into the peritoneum of mice facilitated the resolution of zymosan A-induced peritonitis. 15d-PGJ
administration reduced the number of total leukocytes and attenuated polymorphonuclear leukocyte infiltration. Furthermore, 15d-PGJ
increased the proportion of macrophages engulfing apoptotic neutrophils, a process called efferocytosis. In addition, when the thioglycollate-elicited mouse peritoneal macrophages were stimulated with 15d-PGJ
, their efferocytic activity was amplified. In another experiment, RAW264.7 murine macrophages exposed to 15d-PGJ
conducted phagocytic clearance of apoptotic cells to a greater extent than the control cells. Under these conditions, expression of CD36 and heme oxygenase-1 (HO-1) was enhanced along with increased accumulation of the nuclear factor E2-related factor 2 (Nrf2) in the nucleus. Knockdown of Nrf2 abolished 15d-PGJ
-induced expression of CD36 and HO-1, and silencing of CD36 and HO-1 attenuated 15d-PGJ
-induced efferocytosis. Moreover, peritoneal macrophages isolated from Nrf2-null mice failed to upregulate 15d-PGJ
-induced expression of CD36 and HO-1 and to mediate efferocytosis. Unlike 15d-PGJ
, its nonelectrophilic analog 9,10-dihydro-15d-PGJ
lacking the α,β-unsaturated carbonyl group could not induce CD36 expression and efferocytosis.
15d-PGJ
, as one of the terminal products of cyclooxygenase-2, exerts proresolving effects through induction of efferocytosis. The results of this study suggest that 15d-PGJ
possesses a therapeutic value in the management of inflammatory disorders.
15d-PGJ
facilitates resolution of inflammation by inducing Nrf2-induced expression of CD36 and HO-1 in macrophages. Antioxid. Redox Signal. 27, 1412-1431.</description><subject>Animals</subject><subject>CD36 Antigens - metabolism</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Humans</subject><subject>Jurkat Cells</subject><subject>Macrophages - cytology</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Mice</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Peritonitis - chemically induced</subject><subject>Peritonitis - drug therapy</subject><subject>Phagocytosis</subject><subject>Prostaglandin D2 - administration & dosage</subject><subject>Prostaglandin D2 - analogs & derivatives</subject><subject>Prostaglandin D2 - pharmacology</subject><subject>RAW 264.7 Cells</subject><subject>Zymosan - adverse effects</subject><issn>1523-0864</issn><issn>1557-7716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kM9OwkAQxjdGI4gevZp9ABf3T3e3PRoogiFiDJ6bbTsLmNKSXWrgPbz5Tj6TSxBPM_nmyzczP4RuGe0zGicPxvk-p0z1lZbRGeoyKTXRmqnzQ88FobGKOujK-w9KKWeMXqIOj0USxzzqom8myRCa3Z78fGHG71mEyatr_NYsKlOXqxo_Y47THbitx2HgwDfV56pe4NRaKII4X7qmXSzxS1tUYBwemWLbOJxy8gaV2UJ5UjiZ1GVbBCHdbUKOXzU1biweDIXCYRcewxrwbLdfQG08EHaNLqypPNz81R56H6XzwZhMZ0-TweOUFIzKiEgZDuG0VCovC5XEOjEWpJBCQ25FYg3TogSTS6tKynROY4iltjk3eZEkUS56iBxzi_C4d2CzjVutjdtnjGYHyFmAnB0gZwfIwX939G_afA3lv_tEVfwCrLx4JA</recordid><startdate>20171210</startdate><enddate>20171210</enddate><creator>Kim, Wonki</creator><creator>Lee, Ha-Na</creator><creator>Jang, Jeong-Hoon</creator><creator>Kim, Seung Hyeon</creator><creator>Lee, Yeon-Hwa</creator><creator>Hahn, Young-Il</creator><creator>Ngo, Hoang-Kieu-Chi</creator><creator>Choi, Yeonseo</creator><creator>Joe, Yeonsoo</creator><creator>Chung, Hun Taeg</creator><creator>Chen, Yingqing</creator><creator>Cha, Young Nam</creator><creator>Surh, Young-Joon</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20171210</creationdate><title>15-Deoxy-Δ 12,14 -Prostaglandin J 2 Exerts Proresolving Effects Through Nuclear Factor E2-Related Factor 2-Induced Expression of CD36 and Heme Oxygenase-1</title><author>Kim, Wonki ; Lee, Ha-Na ; Jang, Jeong-Hoon ; Kim, Seung Hyeon ; Lee, Yeon-Hwa ; Hahn, Young-Il ; Ngo, Hoang-Kieu-Chi ; Choi, Yeonseo ; Joe, Yeonsoo ; Chung, Hun Taeg ; Chen, Yingqing ; Cha, Young Nam ; Surh, Young-Joon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c1054-55fec20d66bdc69879afe53537ebf39fa173deab5f6d017b08e857fb2abc994b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>CD36 Antigens - metabolism</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Humans</topic><topic>Jurkat Cells</topic><topic>Macrophages - cytology</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Peritonitis - chemically induced</topic><topic>Peritonitis - drug therapy</topic><topic>Phagocytosis</topic><topic>Prostaglandin D2 - administration & dosage</topic><topic>Prostaglandin D2 - analogs & derivatives</topic><topic>Prostaglandin D2 - pharmacology</topic><topic>RAW 264.7 Cells</topic><topic>Zymosan - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Wonki</creatorcontrib><creatorcontrib>Lee, Ha-Na</creatorcontrib><creatorcontrib>Jang, Jeong-Hoon</creatorcontrib><creatorcontrib>Kim, Seung Hyeon</creatorcontrib><creatorcontrib>Lee, Yeon-Hwa</creatorcontrib><creatorcontrib>Hahn, Young-Il</creatorcontrib><creatorcontrib>Ngo, Hoang-Kieu-Chi</creatorcontrib><creatorcontrib>Choi, Yeonseo</creatorcontrib><creatorcontrib>Joe, Yeonsoo</creatorcontrib><creatorcontrib>Chung, Hun Taeg</creatorcontrib><creatorcontrib>Chen, Yingqing</creatorcontrib><creatorcontrib>Cha, Young Nam</creatorcontrib><creatorcontrib>Surh, Young-Joon</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Antioxidants & redox signaling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Wonki</au><au>Lee, Ha-Na</au><au>Jang, Jeong-Hoon</au><au>Kim, Seung Hyeon</au><au>Lee, Yeon-Hwa</au><au>Hahn, Young-Il</au><au>Ngo, Hoang-Kieu-Chi</au><au>Choi, Yeonseo</au><au>Joe, Yeonsoo</au><au>Chung, Hun Taeg</au><au>Chen, Yingqing</au><au>Cha, Young Nam</au><au>Surh, Young-Joon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>15-Deoxy-Δ 12,14 -Prostaglandin J 2 Exerts Proresolving Effects Through Nuclear Factor E2-Related Factor 2-Induced Expression of CD36 and Heme Oxygenase-1</atitle><jtitle>Antioxidants & redox signaling</jtitle><addtitle>Antioxid Redox Signal</addtitle><date>2017-12-10</date><risdate>2017</risdate><volume>27</volume><issue>17</issue><spage>1412</spage><epage>1431</epage><pages>1412-1431</pages><issn>1523-0864</issn><eissn>1557-7716</eissn><abstract>15-Deoxy-Δ
-prostaglandin J
(15d-PGJ
) has been shown to rescue cells from inflammatory insults and to participate in the resolution of acute inflammation. In this study, we investigated molecular mechanisms underlying proresolving effects of 15d-PGJ
.
15d-PGJ
injected into the peritoneum of mice facilitated the resolution of zymosan A-induced peritonitis. 15d-PGJ
administration reduced the number of total leukocytes and attenuated polymorphonuclear leukocyte infiltration. Furthermore, 15d-PGJ
increased the proportion of macrophages engulfing apoptotic neutrophils, a process called efferocytosis. In addition, when the thioglycollate-elicited mouse peritoneal macrophages were stimulated with 15d-PGJ
, their efferocytic activity was amplified. In another experiment, RAW264.7 murine macrophages exposed to 15d-PGJ
conducted phagocytic clearance of apoptotic cells to a greater extent than the control cells. Under these conditions, expression of CD36 and heme oxygenase-1 (HO-1) was enhanced along with increased accumulation of the nuclear factor E2-related factor 2 (Nrf2) in the nucleus. Knockdown of Nrf2 abolished 15d-PGJ
-induced expression of CD36 and HO-1, and silencing of CD36 and HO-1 attenuated 15d-PGJ
-induced efferocytosis. Moreover, peritoneal macrophages isolated from Nrf2-null mice failed to upregulate 15d-PGJ
-induced expression of CD36 and HO-1 and to mediate efferocytosis. Unlike 15d-PGJ
, its nonelectrophilic analog 9,10-dihydro-15d-PGJ
lacking the α,β-unsaturated carbonyl group could not induce CD36 expression and efferocytosis.
15d-PGJ
, as one of the terminal products of cyclooxygenase-2, exerts proresolving effects through induction of efferocytosis. The results of this study suggest that 15d-PGJ
possesses a therapeutic value in the management of inflammatory disorders.
15d-PGJ
facilitates resolution of inflammation by inducing Nrf2-induced expression of CD36 and HO-1 in macrophages. Antioxid. Redox Signal. 27, 1412-1431.</abstract><cop>United States</cop><pmid>28398824</pmid><doi>10.1089/ars.2016.6754</doi><tpages>20</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1523-0864 |
| ispartof | Antioxidants & redox signaling, 2017-12, Vol.27 (17), p.1412-1431 |
| issn | 1523-0864 1557-7716 |
| language | eng |
| recordid | cdi_crossref_primary_10_1089_ars_2016_6754 |
| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Animals CD36 Antigens - metabolism Gene Expression Regulation - drug effects Heme Oxygenase-1 - metabolism Humans Jurkat Cells Macrophages - cytology Macrophages - drug effects Macrophages - metabolism Mice NF-E2-Related Factor 2 - metabolism Peritonitis - chemically induced Peritonitis - drug therapy Phagocytosis Prostaglandin D2 - administration & dosage Prostaglandin D2 - analogs & derivatives Prostaglandin D2 - pharmacology RAW 264.7 Cells Zymosan - adverse effects |
| title | 15-Deoxy-Δ 12,14 -Prostaglandin J 2 Exerts Proresolving Effects Through Nuclear Factor E2-Related Factor 2-Induced Expression of CD36 and Heme Oxygenase-1 |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-15T03%3A34%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=15-Deoxy-%CE%94%2012,14%20-Prostaglandin%20J%202%20Exerts%20Proresolving%20Effects%20Through%20Nuclear%20Factor%20E2-Related%20Factor%202-Induced%20Expression%20of%20CD36%20and%20Heme%20Oxygenase-1&rft.jtitle=Antioxidants%20&%20redox%20signaling&rft.au=Kim,%20Wonki&rft.date=2017-12-10&rft.volume=27&rft.issue=17&rft.spage=1412&rft.epage=1431&rft.pages=1412-1431&rft.issn=1523-0864&rft.eissn=1557-7716&rft_id=info:doi/10.1089/ars.2016.6754&rft_dat=%3Cpubmed_cross%3E28398824%3C/pubmed_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/28398824&rfr_iscdi=true |