1[alpha],25-Dihydroxyvitamin D3 Ameliorates Seawater Aspiration-Induced Lung Injury By Inhibiting The Translocation Of NF-[kappa]B and RhoA
Our previous study have reported that 1[alpha],25-Dihydroxyvitamin D3 (calcitriol) suppresses seawater aspiration-induced ALI in vitro and in vivo. We also have confirmed that treatment with calcitriol ameliorates seawater aspiration-induced inflammation and pulmonary edema via the inhibition of NF-...
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Veröffentlicht in: | Inflammation 2017-06, Vol.40 (3), p.832 |
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description | Our previous study have reported that 1[alpha],25-Dihydroxyvitamin D3 (calcitriol) suppresses seawater aspiration-induced ALI in vitro and in vivo. We also have confirmed that treatment with calcitriol ameliorates seawater aspiration-induced inflammation and pulmonary edema via the inhibition of NF-[kappa]B and RhoA/Rho kinase pathway activation. In our further work, we investigated the effect of calcitriol on nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in vitro. A549 cells and rat pulmonary microvascular endothelial cells (RPMVECs) were cultured with calcitriol or not for 48 h and then stimulated with 25% seawater for 40 min. After these treatments, cells were collected and performed with immunofluorescent staining to observe the translocation of NF-[kappa]B and RhoA and the cytoskeleton remodeling. In vitro, seawater stimulation activates nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in A549 cells. In addition, seawater administration also induced cytoskeleton remodeling in A549 cells and RPMVECs. However, pretreatment with calcitriol significantly inhibited the activation of NF-[kappa]B and RhoA/Rho kinase pathways, as demonstrated by the reduced nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in A549 cells. Meanwhile, treatment of calcitriol also regulated the cytoskeleton remodeling in both A549 cells and RPMVECs. These results demonstrated that treatment with calcitriol ameliorates seawater aspiration-induced ALI via inhibition of nuclear translocation of NF-[kappa]B and membrane translocation of RhoA and protection of alveolar epithelial and pulmonary microvascular endothelial barrier. |
doi_str_mv | 10.1007/s10753-017-0527-3 |
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We also have confirmed that treatment with calcitriol ameliorates seawater aspiration-induced inflammation and pulmonary edema via the inhibition of NF-[kappa]B and RhoA/Rho kinase pathway activation. In our further work, we investigated the effect of calcitriol on nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in vitro. A549 cells and rat pulmonary microvascular endothelial cells (RPMVECs) were cultured with calcitriol or not for 48 h and then stimulated with 25% seawater for 40 min. After these treatments, cells were collected and performed with immunofluorescent staining to observe the translocation of NF-[kappa]B and RhoA and the cytoskeleton remodeling. In vitro, seawater stimulation activates nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in A549 cells. In addition, seawater administration also induced cytoskeleton remodeling in A549 cells and RPMVECs. However, pretreatment with calcitriol significantly inhibited the activation of NF-[kappa]B and RhoA/Rho kinase pathways, as demonstrated by the reduced nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in A549 cells. Meanwhile, treatment of calcitriol also regulated the cytoskeleton remodeling in both A549 cells and RPMVECs. These results demonstrated that treatment with calcitriol ameliorates seawater aspiration-induced ALI via inhibition of nuclear translocation of NF-[kappa]B and membrane translocation of RhoA and protection of alveolar epithelial and pulmonary microvascular endothelial barrier.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-017-0527-3</identifier><language>eng</language><publisher>New York: Springer Nature B.V</publisher><subject>Alveoli ; Calcitriol ; Cytoskeleton ; Edema ; Endothelial cells ; Kinases ; Lungs ; Microvasculature ; NF-κB protein ; Nuclear transport ; Rho-associated kinase ; RhoA protein ; Seawater ; Vitamin D3</subject><ispartof>Inflammation, 2017-06, Vol.40 (3), p.832</ispartof><rights>Inflammation is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Zhang, Minlong</creatorcontrib><creatorcontrib>Jin, Faguang</creatorcontrib><title>1[alpha],25-Dihydroxyvitamin D3 Ameliorates Seawater Aspiration-Induced Lung Injury By Inhibiting The Translocation Of NF-[kappa]B and RhoA</title><title>Inflammation</title><description>Our previous study have reported that 1[alpha],25-Dihydroxyvitamin D3 (calcitriol) suppresses seawater aspiration-induced ALI in vitro and in vivo. We also have confirmed that treatment with calcitriol ameliorates seawater aspiration-induced inflammation and pulmonary edema via the inhibition of NF-[kappa]B and RhoA/Rho kinase pathway activation. In our further work, we investigated the effect of calcitriol on nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in vitro. A549 cells and rat pulmonary microvascular endothelial cells (RPMVECs) were cultured with calcitriol or not for 48 h and then stimulated with 25% seawater for 40 min. After these treatments, cells were collected and performed with immunofluorescent staining to observe the translocation of NF-[kappa]B and RhoA and the cytoskeleton remodeling. In vitro, seawater stimulation activates nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in A549 cells. In addition, seawater administration also induced cytoskeleton remodeling in A549 cells and RPMVECs. However, pretreatment with calcitriol significantly inhibited the activation of NF-[kappa]B and RhoA/Rho kinase pathways, as demonstrated by the reduced nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in A549 cells. Meanwhile, treatment of calcitriol also regulated the cytoskeleton remodeling in both A549 cells and RPMVECs. These results demonstrated that treatment with calcitriol ameliorates seawater aspiration-induced ALI via inhibition of nuclear translocation of NF-[kappa]B and membrane translocation of RhoA and protection of alveolar epithelial and pulmonary microvascular endothelial barrier.</description><subject>Alveoli</subject><subject>Calcitriol</subject><subject>Cytoskeleton</subject><subject>Edema</subject><subject>Endothelial cells</subject><subject>Kinases</subject><subject>Lungs</subject><subject>Microvasculature</subject><subject>NF-κB protein</subject><subject>Nuclear transport</subject><subject>Rho-associated kinase</subject><subject>RhoA protein</subject><subject>Seawater</subject><subject>Vitamin D3</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNqNj99KwzAYxYMoWKcP4N0H3hr90timveycw8FQ0N6NMeKa2dQuqUmr9hl8aYP4AF6dH-fPxSHknOEVQxTXnqFIOEUmKCaxoPyARCwRnMaJSA9JhDxFyvNcHJMT7xtEzPKMR-SbrWTb1XJ9GSd0puuxcvZr_NC93GsDMw7FXrXaOtkrD89KfgZwUPhOB0tbQxemGraqguVgXmFhmsGNMB0D1fpF9zqYZa2gdNL41m5_N_C4g4c5Xb3JrpPrKUhTwVNti1NytJOtV2d_OiEX87vy9p52zr4Pyvebxg7OhGjDsnCFZSm_4f9r_QBAhlnR</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>Zhang, Minlong</creator><creator>Jin, Faguang</creator><general>Springer Nature B.V</general><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20170601</creationdate><title>1[alpha],25-Dihydroxyvitamin D3 Ameliorates Seawater Aspiration-Induced Lung Injury By Inhibiting The Translocation Of NF-[kappa]B and RhoA</title><author>Zhang, Minlong ; Jin, Faguang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_18997186343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Alveoli</topic><topic>Calcitriol</topic><topic>Cytoskeleton</topic><topic>Edema</topic><topic>Endothelial cells</topic><topic>Kinases</topic><topic>Lungs</topic><topic>Microvasculature</topic><topic>NF-κB protein</topic><topic>Nuclear transport</topic><topic>Rho-associated kinase</topic><topic>RhoA protein</topic><topic>Seawater</topic><topic>Vitamin D3</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Minlong</creatorcontrib><creatorcontrib>Jin, Faguang</creatorcontrib><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Minlong</au><au>Jin, Faguang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>1[alpha],25-Dihydroxyvitamin D3 Ameliorates Seawater Aspiration-Induced Lung Injury By Inhibiting The Translocation Of NF-[kappa]B and RhoA</atitle><jtitle>Inflammation</jtitle><date>2017-06-01</date><risdate>2017</risdate><volume>40</volume><issue>3</issue><spage>832</spage><pages>832-</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Our previous study have reported that 1[alpha],25-Dihydroxyvitamin D3 (calcitriol) suppresses seawater aspiration-induced ALI in vitro and in vivo. We also have confirmed that treatment with calcitriol ameliorates seawater aspiration-induced inflammation and pulmonary edema via the inhibition of NF-[kappa]B and RhoA/Rho kinase pathway activation. In our further work, we investigated the effect of calcitriol on nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in vitro. A549 cells and rat pulmonary microvascular endothelial cells (RPMVECs) were cultured with calcitriol or not for 48 h and then stimulated with 25% seawater for 40 min. After these treatments, cells were collected and performed with immunofluorescent staining to observe the translocation of NF-[kappa]B and RhoA and the cytoskeleton remodeling. In vitro, seawater stimulation activates nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in A549 cells. In addition, seawater administration also induced cytoskeleton remodeling in A549 cells and RPMVECs. However, pretreatment with calcitriol significantly inhibited the activation of NF-[kappa]B and RhoA/Rho kinase pathways, as demonstrated by the reduced nuclear translocation of NF-[kappa]B and membrane translocation of RhoA in A549 cells. Meanwhile, treatment of calcitriol also regulated the cytoskeleton remodeling in both A549 cells and RPMVECs. These results demonstrated that treatment with calcitriol ameliorates seawater aspiration-induced ALI via inhibition of nuclear translocation of NF-[kappa]B and membrane translocation of RhoA and protection of alveolar epithelial and pulmonary microvascular endothelial barrier.</abstract><cop>New York</cop><pub>Springer Nature B.V</pub><doi>10.1007/s10753-017-0527-3</doi></addata></record> |
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subjects | Alveoli Calcitriol Cytoskeleton Edema Endothelial cells Kinases Lungs Microvasculature NF-κB protein Nuclear transport Rho-associated kinase RhoA protein Seawater Vitamin D3 |
title | 1[alpha],25-Dihydroxyvitamin D3 Ameliorates Seawater Aspiration-Induced Lung Injury By Inhibiting The Translocation Of NF-[kappa]B and RhoA |
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