Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation
Peroxisome proliferator-activated receptor (PPAR)-γ is highly expressed in human and rodent placentas. Nevertheless, its function remains obscure. The present study investigated the effects of rosiglitazone, a PPAR-γ agonist, on LPS-induced fetal death. All pregnant mice except controls were intrape...
Gespeichert in:
| Veröffentlicht in: | Molecular and cellular endocrinology 2016-03, Vol.423, p.51-59 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 59 |
|---|---|
| container_issue | |
| container_start_page | 51 |
| container_title | Molecular and cellular endocrinology |
| container_volume | 423 |
| creator | Bo, Qing-Li Chen, Yuan-Hua Yu, Zhen Fu, Lin Zhou, Yan Zhang, Gui-Bin Wang, Hua Zhang, Zhi-Hui Xu, De-Xiang |
| description | Peroxisome proliferator-activated receptor (PPAR)-γ is highly expressed in human and rodent placentas. Nevertheless, its function remains obscure. The present study investigated the effects of rosiglitazone, a PPAR-γ agonist, on LPS-induced fetal death. All pregnant mice except controls were intraperitoneally injected with LPS (150 μg/kg) daily from gestational day (GD)15 to GD17. As expected, maternal LPS injection caused placental inflammation and resulted in 63.6% fetal death in dams that completed the pregnancy. Interestingly, LPS-induced fetal mortality was reduced to 16.0% when pregnant mice were pretreated with RSG. Additional experiment showed that rosiglitazone pretreatment inhibited LPS-induced expressions of tumor necrosis factor (Tnf)-α, interleukin (Il)-1β, Il-6, macrophage inflammatory protein (Mip)-2 and keratinocyte-derived chemokine (Kc) in mouse placenta. Although rosiglitazone had little effect on LPS-evoked elevation of IL-10 in amniotic fluid, it alleviated LPS-evoked release of TNF-α and MIP-2 in amniotic fluid. Further analysis showed that pretreatment with rosiglitazone, which activated placental PPAR-γ signaling, simultaneously suppressed LPS-evoked nuclear factor kappa B (NF-κB) activation and blocked nuclear translocation of NF-κB p65 and p50 subunits in trophoblast giant cells of the labyrinth layer. These results provide a mechanistic explanation for PPAR-γ-mediated anti-inflammatory activity in the placentas. Overall, the present study provides additional evidence for roles of PPAR-γ as an important regulator of placental inflammation.
•RSG pretreatment alleviates LPS-induced fetal death in mice.•RSG activates PPAR-γ signaling in mouse placenta.•RSG pretreatment inhibits LPS-evoked placental NF-κB activation.•RSG blocks LPS-induced nuclear translocation of placental NF-κB p65 and p50 subunits.•RSG inhibits LPS-induced placental inflammation through activating PPAR-γ signaling. |
| doi_str_mv | 10.1016/j.mce.2016.01.004 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1816018505</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0303720716300041</els_id><sourcerecordid>1816018505</sourcerecordid><originalsourceid>FETCH-LOGICAL-c456t-dc57aadb7fa3254cf56a3b1e277ec204f06c84188e8defb3a588f71727aaa0803</originalsourceid><addsrcrecordid>eNp9kE2LFDEQhoMo7rj6A7xIH710W0l_JOBJFr9gQRA9h-qkMpOhO2mTtLCC_90ss3r0lAo870vVw9hLDh0HPr05d6uhTtSxA94BDI_YgSspWgWjfMwO0EPfSgHyij3L-QwAchTqKbsSk5S9FOrAfn-N2R8XX_BXDNRsiUoiLCuFUj-xkCm5wSP6kEuz-C1ucbnLaMwJk7fU-mB3Q7ZxVHBpLK0-U1NOKe7HU-PDyc---HBstgVN7ayMD27BdcXiY3jOnjhcMr14eK_Z9w_vv918am-_fPx88-62NcM4ldaaUSLaWTrsxTgYN07Yz5yElGQEDA4mowauFClLbu5xVMpJLkVNISjor9nrS2896cdOuei6p6FlwUBxz5orPgFXI4wV5RfUpJhzIqe35FdMd5qDvreuz7pa1_fWNXBdrdfMq4f6fV7J_kv81VyBtxeA6pE_PSWdjadQxflUDWsb_X_q_wA52JcK</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1816018505</pqid></control><display><type>article</type><title>Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Bo, Qing-Li ; Chen, Yuan-Hua ; Yu, Zhen ; Fu, Lin ; Zhou, Yan ; Zhang, Gui-Bin ; Wang, Hua ; Zhang, Zhi-Hui ; Xu, De-Xiang</creator><creatorcontrib>Bo, Qing-Li ; Chen, Yuan-Hua ; Yu, Zhen ; Fu, Lin ; Zhou, Yan ; Zhang, Gui-Bin ; Wang, Hua ; Zhang, Zhi-Hui ; Xu, De-Xiang</creatorcontrib><description>Peroxisome proliferator-activated receptor (PPAR)-γ is highly expressed in human and rodent placentas. Nevertheless, its function remains obscure. The present study investigated the effects of rosiglitazone, a PPAR-γ agonist, on LPS-induced fetal death. All pregnant mice except controls were intraperitoneally injected with LPS (150 μg/kg) daily from gestational day (GD)15 to GD17. As expected, maternal LPS injection caused placental inflammation and resulted in 63.6% fetal death in dams that completed the pregnancy. Interestingly, LPS-induced fetal mortality was reduced to 16.0% when pregnant mice were pretreated with RSG. Additional experiment showed that rosiglitazone pretreatment inhibited LPS-induced expressions of tumor necrosis factor (Tnf)-α, interleukin (Il)-1β, Il-6, macrophage inflammatory protein (Mip)-2 and keratinocyte-derived chemokine (Kc) in mouse placenta. Although rosiglitazone had little effect on LPS-evoked elevation of IL-10 in amniotic fluid, it alleviated LPS-evoked release of TNF-α and MIP-2 in amniotic fluid. Further analysis showed that pretreatment with rosiglitazone, which activated placental PPAR-γ signaling, simultaneously suppressed LPS-evoked nuclear factor kappa B (NF-κB) activation and blocked nuclear translocation of NF-κB p65 and p50 subunits in trophoblast giant cells of the labyrinth layer. These results provide a mechanistic explanation for PPAR-γ-mediated anti-inflammatory activity in the placentas. Overall, the present study provides additional evidence for roles of PPAR-γ as an important regulator of placental inflammation.
•RSG pretreatment alleviates LPS-induced fetal death in mice.•RSG activates PPAR-γ signaling in mouse placenta.•RSG pretreatment inhibits LPS-evoked placental NF-κB activation.•RSG blocks LPS-induced nuclear translocation of placental NF-κB p65 and p50 subunits.•RSG inhibits LPS-induced placental inflammation through activating PPAR-γ signaling.</description><identifier>ISSN: 0303-7207</identifier><identifier>EISSN: 1872-8057</identifier><identifier>DOI: 10.1016/j.mce.2016.01.004</identifier><identifier>PMID: 26773728</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Active Transport, Cell Nucleus ; Animals ; Anti-Inflammatory Agents - administration & dosage ; Cellular ; Chemokines - blood ; Death ; Drug Evaluation, Preclinical ; Female ; Fetal death ; Fetal Death - prevention & control ; Fluid dynamics ; Fluid flow ; Fluids ; Inflammation ; Lipopolysaccharide ; Lipopolysaccharides - pharmacology ; Male ; Mice ; Mice, Inbred ICR ; NF-kappa B - metabolism ; Peroxisome proliferator-activated receptor-γ ; Placenta ; Placenta - drug effects ; Placenta - immunology ; Placenta - metabolism ; PPAR gamma - metabolism ; Pregnancy ; Pretreatment ; Rosiglitazone ; Signal Transduction ; Thiazolidinediones - administration & dosage</subject><ispartof>Molecular and cellular endocrinology, 2016-03, Vol.423, p.51-59</ispartof><rights>2016 Elsevier Ireland Ltd</rights><rights>Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c456t-dc57aadb7fa3254cf56a3b1e277ec204f06c84188e8defb3a588f71727aaa0803</citedby><cites>FETCH-LOGICAL-c456t-dc57aadb7fa3254cf56a3b1e277ec204f06c84188e8defb3a588f71727aaa0803</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0303720716300041$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26773728$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bo, Qing-Li</creatorcontrib><creatorcontrib>Chen, Yuan-Hua</creatorcontrib><creatorcontrib>Yu, Zhen</creatorcontrib><creatorcontrib>Fu, Lin</creatorcontrib><creatorcontrib>Zhou, Yan</creatorcontrib><creatorcontrib>Zhang, Gui-Bin</creatorcontrib><creatorcontrib>Wang, Hua</creatorcontrib><creatorcontrib>Zhang, Zhi-Hui</creatorcontrib><creatorcontrib>Xu, De-Xiang</creatorcontrib><title>Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation</title><title>Molecular and cellular endocrinology</title><addtitle>Mol Cell Endocrinol</addtitle><description>Peroxisome proliferator-activated receptor (PPAR)-γ is highly expressed in human and rodent placentas. Nevertheless, its function remains obscure. The present study investigated the effects of rosiglitazone, a PPAR-γ agonist, on LPS-induced fetal death. All pregnant mice except controls were intraperitoneally injected with LPS (150 μg/kg) daily from gestational day (GD)15 to GD17. As expected, maternal LPS injection caused placental inflammation and resulted in 63.6% fetal death in dams that completed the pregnancy. Interestingly, LPS-induced fetal mortality was reduced to 16.0% when pregnant mice were pretreated with RSG. Additional experiment showed that rosiglitazone pretreatment inhibited LPS-induced expressions of tumor necrosis factor (Tnf)-α, interleukin (Il)-1β, Il-6, macrophage inflammatory protein (Mip)-2 and keratinocyte-derived chemokine (Kc) in mouse placenta. Although rosiglitazone had little effect on LPS-evoked elevation of IL-10 in amniotic fluid, it alleviated LPS-evoked release of TNF-α and MIP-2 in amniotic fluid. Further analysis showed that pretreatment with rosiglitazone, which activated placental PPAR-γ signaling, simultaneously suppressed LPS-evoked nuclear factor kappa B (NF-κB) activation and blocked nuclear translocation of NF-κB p65 and p50 subunits in trophoblast giant cells of the labyrinth layer. These results provide a mechanistic explanation for PPAR-γ-mediated anti-inflammatory activity in the placentas. Overall, the present study provides additional evidence for roles of PPAR-γ as an important regulator of placental inflammation.
•RSG pretreatment alleviates LPS-induced fetal death in mice.•RSG activates PPAR-γ signaling in mouse placenta.•RSG pretreatment inhibits LPS-evoked placental NF-κB activation.•RSG blocks LPS-induced nuclear translocation of placental NF-κB p65 and p50 subunits.•RSG inhibits LPS-induced placental inflammation through activating PPAR-γ signaling.</description><subject>Active Transport, Cell Nucleus</subject><subject>Animals</subject><subject>Anti-Inflammatory Agents - administration & dosage</subject><subject>Cellular</subject><subject>Chemokines - blood</subject><subject>Death</subject><subject>Drug Evaluation, Preclinical</subject><subject>Female</subject><subject>Fetal death</subject><subject>Fetal Death - prevention & control</subject><subject>Fluid dynamics</subject><subject>Fluid flow</subject><subject>Fluids</subject><subject>Inflammation</subject><subject>Lipopolysaccharide</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>NF-kappa B - metabolism</subject><subject>Peroxisome proliferator-activated receptor-γ</subject><subject>Placenta</subject><subject>Placenta - drug effects</subject><subject>Placenta - immunology</subject><subject>Placenta - metabolism</subject><subject>PPAR gamma - metabolism</subject><subject>Pregnancy</subject><subject>Pretreatment</subject><subject>Rosiglitazone</subject><subject>Signal Transduction</subject><subject>Thiazolidinediones - administration & dosage</subject><issn>0303-7207</issn><issn>1872-8057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE2LFDEQhoMo7rj6A7xIH710W0l_JOBJFr9gQRA9h-qkMpOhO2mTtLCC_90ss3r0lAo870vVw9hLDh0HPr05d6uhTtSxA94BDI_YgSspWgWjfMwO0EPfSgHyij3L-QwAchTqKbsSk5S9FOrAfn-N2R8XX_BXDNRsiUoiLCuFUj-xkCm5wSP6kEuz-C1ucbnLaMwJk7fU-mB3Q7ZxVHBpLK0-U1NOKe7HU-PDyc---HBstgVN7ayMD27BdcXiY3jOnjhcMr14eK_Z9w_vv918am-_fPx88-62NcM4ldaaUSLaWTrsxTgYN07Yz5yElGQEDA4mowauFClLbu5xVMpJLkVNISjor9nrS2896cdOuei6p6FlwUBxz5orPgFXI4wV5RfUpJhzIqe35FdMd5qDvreuz7pa1_fWNXBdrdfMq4f6fV7J_kv81VyBtxeA6pE_PSWdjadQxflUDWsb_X_q_wA52JcK</recordid><startdate>20160305</startdate><enddate>20160305</enddate><creator>Bo, Qing-Li</creator><creator>Chen, Yuan-Hua</creator><creator>Yu, Zhen</creator><creator>Fu, Lin</creator><creator>Zhou, Yan</creator><creator>Zhang, Gui-Bin</creator><creator>Wang, Hua</creator><creator>Zhang, Zhi-Hui</creator><creator>Xu, De-Xiang</creator><general>Elsevier Ireland Ltd</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>7U5</scope><scope>8FD</scope><scope>L7M</scope></search><sort><creationdate>20160305</creationdate><title>Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation</title><author>Bo, Qing-Li ; Chen, Yuan-Hua ; Yu, Zhen ; Fu, Lin ; Zhou, Yan ; Zhang, Gui-Bin ; Wang, Hua ; Zhang, Zhi-Hui ; Xu, De-Xiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c456t-dc57aadb7fa3254cf56a3b1e277ec204f06c84188e8defb3a588f71727aaa0803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Active Transport, Cell Nucleus</topic><topic>Animals</topic><topic>Anti-Inflammatory Agents - administration & dosage</topic><topic>Cellular</topic><topic>Chemokines - blood</topic><topic>Death</topic><topic>Drug Evaluation, Preclinical</topic><topic>Female</topic><topic>Fetal death</topic><topic>Fetal Death - prevention & control</topic><topic>Fluid dynamics</topic><topic>Fluid flow</topic><topic>Fluids</topic><topic>Inflammation</topic><topic>Lipopolysaccharide</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>NF-kappa B - metabolism</topic><topic>Peroxisome proliferator-activated receptor-γ</topic><topic>Placenta</topic><topic>Placenta - drug effects</topic><topic>Placenta - immunology</topic><topic>Placenta - metabolism</topic><topic>PPAR gamma - metabolism</topic><topic>Pregnancy</topic><topic>Pretreatment</topic><topic>Rosiglitazone</topic><topic>Signal Transduction</topic><topic>Thiazolidinediones - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bo, Qing-Li</creatorcontrib><creatorcontrib>Chen, Yuan-Hua</creatorcontrib><creatorcontrib>Yu, Zhen</creatorcontrib><creatorcontrib>Fu, Lin</creatorcontrib><creatorcontrib>Zhou, Yan</creatorcontrib><creatorcontrib>Zhang, Gui-Bin</creatorcontrib><creatorcontrib>Wang, Hua</creatorcontrib><creatorcontrib>Zhang, Zhi-Hui</creatorcontrib><creatorcontrib>Xu, De-Xiang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bo, Qing-Li</au><au>Chen, Yuan-Hua</au><au>Yu, Zhen</au><au>Fu, Lin</au><au>Zhou, Yan</au><au>Zhang, Gui-Bin</au><au>Wang, Hua</au><au>Zhang, Zhi-Hui</au><au>Xu, De-Xiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2016-03-05</date><risdate>2016</risdate><volume>423</volume><spage>51</spage><epage>59</epage><pages>51-59</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>Peroxisome proliferator-activated receptor (PPAR)-γ is highly expressed in human and rodent placentas. Nevertheless, its function remains obscure. The present study investigated the effects of rosiglitazone, a PPAR-γ agonist, on LPS-induced fetal death. All pregnant mice except controls were intraperitoneally injected with LPS (150 μg/kg) daily from gestational day (GD)15 to GD17. As expected, maternal LPS injection caused placental inflammation and resulted in 63.6% fetal death in dams that completed the pregnancy. Interestingly, LPS-induced fetal mortality was reduced to 16.0% when pregnant mice were pretreated with RSG. Additional experiment showed that rosiglitazone pretreatment inhibited LPS-induced expressions of tumor necrosis factor (Tnf)-α, interleukin (Il)-1β, Il-6, macrophage inflammatory protein (Mip)-2 and keratinocyte-derived chemokine (Kc) in mouse placenta. Although rosiglitazone had little effect on LPS-evoked elevation of IL-10 in amniotic fluid, it alleviated LPS-evoked release of TNF-α and MIP-2 in amniotic fluid. Further analysis showed that pretreatment with rosiglitazone, which activated placental PPAR-γ signaling, simultaneously suppressed LPS-evoked nuclear factor kappa B (NF-κB) activation and blocked nuclear translocation of NF-κB p65 and p50 subunits in trophoblast giant cells of the labyrinth layer. These results provide a mechanistic explanation for PPAR-γ-mediated anti-inflammatory activity in the placentas. Overall, the present study provides additional evidence for roles of PPAR-γ as an important regulator of placental inflammation.
•RSG pretreatment alleviates LPS-induced fetal death in mice.•RSG activates PPAR-γ signaling in mouse placenta.•RSG pretreatment inhibits LPS-evoked placental NF-κB activation.•RSG blocks LPS-induced nuclear translocation of placental NF-κB p65 and p50 subunits.•RSG inhibits LPS-induced placental inflammation through activating PPAR-γ signaling.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>26773728</pmid><doi>10.1016/j.mce.2016.01.004</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0303-7207 |
| ispartof | Molecular and cellular endocrinology, 2016-03, Vol.423, p.51-59 |
| issn | 0303-7207 1872-8057 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1816018505 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Active Transport, Cell Nucleus Animals Anti-Inflammatory Agents - administration & dosage Cellular Chemokines - blood Death Drug Evaluation, Preclinical Female Fetal death Fetal Death - prevention & control Fluid dynamics Fluid flow Fluids Inflammation Lipopolysaccharide Lipopolysaccharides - pharmacology Male Mice Mice, Inbred ICR NF-kappa B - metabolism Peroxisome proliferator-activated receptor-γ Placenta Placenta - drug effects Placenta - immunology Placenta - metabolism PPAR gamma - metabolism Pregnancy Pretreatment Rosiglitazone Signal Transduction Thiazolidinediones - administration & dosage |
| title | Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-14T19%3A36%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Rosiglitazone%20pretreatment%20protects%20against%20lipopolysaccharide-induced%20fetal%20demise%20through%20inhibiting%20placental%20inflammation&rft.jtitle=Molecular%20and%20cellular%20endocrinology&rft.au=Bo,%20Qing-Li&rft.date=2016-03-05&rft.volume=423&rft.spage=51&rft.epage=59&rft.pages=51-59&rft.issn=0303-7207&rft.eissn=1872-8057&rft_id=info:doi/10.1016/j.mce.2016.01.004&rft_dat=%3Cproquest_cross%3E1816018505%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1816018505&rft_id=info:pmid/26773728&rft_els_id=S0303720716300041&rfr_iscdi=true |