Effects of prostaglandin lipid mediators on agonist-induced lung endothelial permeability and inflammation
Prostaglandins (PG), the products of cyclooxygenase-mediated conversion of arachidonic acid, become upregulated in many situations including allergic response, inflammation, and injury, and exhibit a variety of biological activities. Previous studies described barrier-enhancing and anti-inflammatory...
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| Veröffentlicht in: | American journal of physiology. Lung cellular and molecular physiology 2017-10, Vol.313 (4), p.L710-L721 |
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| container_title | American journal of physiology. Lung cellular and molecular physiology |
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| creator | Ke, Yunbo Oskolkova, Olga V Sarich, Nicolene Tian, Yufeng Sitikov, Albert Tulapurkar, Mohan E Son, Sophia Birukova, Anna A Birukov, Konstantin G |
| description | Prostaglandins (PG), the products of cyclooxygenase-mediated conversion of arachidonic acid, become upregulated in many situations including allergic response, inflammation, and injury, and exhibit a variety of biological activities. Previous studies described barrier-enhancing and anti-inflammatory effects of PGE
and PGI
on vascular endothelial cells (EC). Yet, the effects of other PG members on EC barrier and inflammatory activation have not been systematically analyzed. This study compared effects of PGE
, PGI
, PGF
, PGA
, PGJ
, and PGD
on human pulmonary EC. EC permeability was assessed by measurements of transendothelial electrical resistance and cell monolayer permeability for FITC-labeled tracer. Anti-inflammatory effects of PGs were evaluated by analysis of expression of adhesion molecule ICAM1 and secretion of soluble ICAM1 and cytokines by EC. PGE
, PGI
, and PGA
exhibited the most potent barrier-enhancing effects and most efficient attenuation of thrombin-induced EC permeability and contractile response, whereas PGI
effectively suppressed thrombin-induced permeability but was less efficient in the attenuation of prolonged EC hyperpermeability caused by interleukin-6 or bacterial wall lipopolysaccharide, LPS. PGD
showed a modest protective effect on the EC inflammatory response, whereas PGF
and PGJ
were without effect on agonist-induced EC barrier dysfunction. In vivo, PGE
, PGI
, and PGA
attenuated LPS-induced lung inflammation, whereas PGF
and PGJ
were without effect. Interestingly, PGD
exhibited a protective effect in the in vivo model of LPS-induced lung injury. This study provides a comprehensive analysis of barrier-protective and anti-inflammatory effects of different prostaglandins on lung EC in vitro and in vivo and identifies PGE
, PGI
, and PGA
as prostaglandins with the most potent protective properties. |
| doi_str_mv | 10.1152/ajplung.00519.2016 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5668565</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1915341838</sourcerecordid><originalsourceid>FETCH-LOGICAL-c496t-6e2acb7f34695454510e22675df9600a8467072e7daae324f9730775bb51ca883</originalsourceid><addsrcrecordid>eNpdkU1rFTEUhoNY7If-ARcScONmbk-SSWayEaRUKxS6qeuQmUluc8kkY5IR-u-bsdeiksUJnPc85-NF6D2BHSGcXurD4tew3wFwIncUiHiFzmqCNoRD-7r-oYUGBPBTdJ7zAaoQQLxBp7QXgjEmztDh2lozloyjxUuKuei912FyAXu3uAnPZnK6xFQFAet9DC6XxoVpHc2Et-7YhCmWB-Od9ngxaTZ6cN6VR1wx2AXr9Tzr4mJ4i06s9tm8O8YL9OPr9f3VTXN79-371ZfbZmylKI0wVI9DZ1krJG_rI2AoFR2frBQAum9FBx013aS1YbS1smPQdXwYOBl137ML9PmZu6xDHX80oSTt1ZLcrNOjitqpfzPBPah9_KW4ED0XvAI-HQEp_lxNLmp2eTS-HsbENSsiCWct6dnW6-N_0kNcU6jrVZXoZS9BbkD6rBrrhXMy9mUYAmqzUh2tVL-tVJuVtejD32u8lPzxjj0Bt6ad3g</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1968989095</pqid></control><display><type>article</type><title>Effects of prostaglandin lipid mediators on agonist-induced lung endothelial permeability and inflammation</title><source>MEDLINE</source><source>American Physiological Society</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Ke, Yunbo ; Oskolkova, Olga V ; Sarich, Nicolene ; Tian, Yufeng ; Sitikov, Albert ; Tulapurkar, Mohan E ; Son, Sophia ; Birukova, Anna A ; Birukov, Konstantin G</creator><creatorcontrib>Ke, Yunbo ; Oskolkova, Olga V ; Sarich, Nicolene ; Tian, Yufeng ; Sitikov, Albert ; Tulapurkar, Mohan E ; Son, Sophia ; Birukova, Anna A ; Birukov, Konstantin G</creatorcontrib><description>Prostaglandins (PG), the products of cyclooxygenase-mediated conversion of arachidonic acid, become upregulated in many situations including allergic response, inflammation, and injury, and exhibit a variety of biological activities. Previous studies described barrier-enhancing and anti-inflammatory effects of PGE
and PGI
on vascular endothelial cells (EC). Yet, the effects of other PG members on EC barrier and inflammatory activation have not been systematically analyzed. This study compared effects of PGE
, PGI
, PGF
, PGA
, PGJ
, and PGD
on human pulmonary EC. EC permeability was assessed by measurements of transendothelial electrical resistance and cell monolayer permeability for FITC-labeled tracer. Anti-inflammatory effects of PGs were evaluated by analysis of expression of adhesion molecule ICAM1 and secretion of soluble ICAM1 and cytokines by EC. PGE
, PGI
, and PGA
exhibited the most potent barrier-enhancing effects and most efficient attenuation of thrombin-induced EC permeability and contractile response, whereas PGI
effectively suppressed thrombin-induced permeability but was less efficient in the attenuation of prolonged EC hyperpermeability caused by interleukin-6 or bacterial wall lipopolysaccharide, LPS. PGD
showed a modest protective effect on the EC inflammatory response, whereas PGF
and PGJ
were without effect on agonist-induced EC barrier dysfunction. In vivo, PGE
, PGI
, and PGA
attenuated LPS-induced lung inflammation, whereas PGF
and PGJ
were without effect. Interestingly, PGD
exhibited a protective effect in the in vivo model of LPS-induced lung injury. This study provides a comprehensive analysis of barrier-protective and anti-inflammatory effects of different prostaglandins on lung EC in vitro and in vivo and identifies PGE
, PGI
, and PGA
as prostaglandins with the most potent protective properties.</description><identifier>ISSN: 1040-0605</identifier><identifier>EISSN: 1522-1504</identifier><identifier>DOI: 10.1152/ajplung.00519.2016</identifier><identifier>PMID: 28663336</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Adhesion tests ; Animals ; Arachidonic acid ; Attenuation ; Bacteria ; Biological effects ; Cell Membrane Permeability - drug effects ; Contractility ; Cytokines ; Effects ; Endothelial cells ; Endothelium ; Endothelium, Vascular - cytology ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - metabolism ; Hemostatics - adverse effects ; Humans ; Hypersensitivity ; In vivo methods and tests ; Inflammation ; Inflammation - chemically induced ; Inflammation - drug therapy ; Inflammation - pathology ; Inflammatory response ; Injury analysis ; Intercellular adhesion molecule 1 ; Intercellular Adhesion Molecule-1 - metabolism ; Interleukin 6 ; Interleukin-6 - metabolism ; Lipids ; Lipopolysaccharides ; Lipopolysaccharides - adverse effects ; Lung Injury - chemically induced ; Lung Injury - drug therapy ; Lung Injury - pathology ; Lungs ; Membrane permeability ; Mice ; Permeability ; Prostacyclin ; Prostaglandin E2 ; Prostaglandin endoperoxide synthase ; Prostaglandins ; Prostaglandins - pharmacology ; Thrombin ; Thrombin - adverse effects</subject><ispartof>American journal of physiology. Lung cellular and molecular physiology, 2017-10, Vol.313 (4), p.L710-L721</ispartof><rights>Copyright © 2017 the American Physiological Society.</rights><rights>Copyright American Physiological Society Oct 2017</rights><rights>Copyright © 2017 the American Physiological Society 2017 American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-6e2acb7f34695454510e22675df9600a8467072e7daae324f9730775bb51ca883</citedby><cites>FETCH-LOGICAL-c496t-6e2acb7f34695454510e22675df9600a8467072e7daae324f9730775bb51ca883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28663336$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ke, Yunbo</creatorcontrib><creatorcontrib>Oskolkova, Olga V</creatorcontrib><creatorcontrib>Sarich, Nicolene</creatorcontrib><creatorcontrib>Tian, Yufeng</creatorcontrib><creatorcontrib>Sitikov, Albert</creatorcontrib><creatorcontrib>Tulapurkar, Mohan E</creatorcontrib><creatorcontrib>Son, Sophia</creatorcontrib><creatorcontrib>Birukova, Anna A</creatorcontrib><creatorcontrib>Birukov, Konstantin G</creatorcontrib><title>Effects of prostaglandin lipid mediators on agonist-induced lung endothelial permeability and inflammation</title><title>American journal of physiology. Lung cellular and molecular physiology</title><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><description>Prostaglandins (PG), the products of cyclooxygenase-mediated conversion of arachidonic acid, become upregulated in many situations including allergic response, inflammation, and injury, and exhibit a variety of biological activities. Previous studies described barrier-enhancing and anti-inflammatory effects of PGE
and PGI
on vascular endothelial cells (EC). Yet, the effects of other PG members on EC barrier and inflammatory activation have not been systematically analyzed. This study compared effects of PGE
, PGI
, PGF
, PGA
, PGJ
, and PGD
on human pulmonary EC. EC permeability was assessed by measurements of transendothelial electrical resistance and cell monolayer permeability for FITC-labeled tracer. Anti-inflammatory effects of PGs were evaluated by analysis of expression of adhesion molecule ICAM1 and secretion of soluble ICAM1 and cytokines by EC. PGE
, PGI
, and PGA
exhibited the most potent barrier-enhancing effects and most efficient attenuation of thrombin-induced EC permeability and contractile response, whereas PGI
effectively suppressed thrombin-induced permeability but was less efficient in the attenuation of prolonged EC hyperpermeability caused by interleukin-6 or bacterial wall lipopolysaccharide, LPS. PGD
showed a modest protective effect on the EC inflammatory response, whereas PGF
and PGJ
were without effect on agonist-induced EC barrier dysfunction. In vivo, PGE
, PGI
, and PGA
attenuated LPS-induced lung inflammation, whereas PGF
and PGJ
were without effect. Interestingly, PGD
exhibited a protective effect in the in vivo model of LPS-induced lung injury. This study provides a comprehensive analysis of barrier-protective and anti-inflammatory effects of different prostaglandins on lung EC in vitro and in vivo and identifies PGE
, PGI
, and PGA
as prostaglandins with the most potent protective properties.</description><subject>Adhesion tests</subject><subject>Animals</subject><subject>Arachidonic acid</subject><subject>Attenuation</subject><subject>Bacteria</subject><subject>Biological effects</subject><subject>Cell Membrane Permeability - drug effects</subject><subject>Contractility</subject><subject>Cytokines</subject><subject>Effects</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Endothelium, Vascular - cytology</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - metabolism</subject><subject>Hemostatics - adverse effects</subject><subject>Humans</subject><subject>Hypersensitivity</subject><subject>In vivo methods and tests</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - pathology</subject><subject>Inflammatory response</subject><subject>Injury analysis</subject><subject>Intercellular adhesion molecule 1</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>Lipids</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - adverse effects</subject><subject>Lung Injury - chemically induced</subject><subject>Lung Injury - drug therapy</subject><subject>Lung Injury - pathology</subject><subject>Lungs</subject><subject>Membrane permeability</subject><subject>Mice</subject><subject>Permeability</subject><subject>Prostacyclin</subject><subject>Prostaglandin E2</subject><subject>Prostaglandin endoperoxide synthase</subject><subject>Prostaglandins</subject><subject>Prostaglandins - pharmacology</subject><subject>Thrombin</subject><subject>Thrombin - adverse effects</subject><issn>1040-0605</issn><issn>1522-1504</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1rFTEUhoNY7If-ARcScONmbk-SSWayEaRUKxS6qeuQmUluc8kkY5IR-u-bsdeiksUJnPc85-NF6D2BHSGcXurD4tew3wFwIncUiHiFzmqCNoRD-7r-oYUGBPBTdJ7zAaoQQLxBp7QXgjEmztDh2lozloyjxUuKuei912FyAXu3uAnPZnK6xFQFAet9DC6XxoVpHc2Et-7YhCmWB-Od9ngxaTZ6cN6VR1wx2AXr9Tzr4mJ4i06s9tm8O8YL9OPr9f3VTXN79-371ZfbZmylKI0wVI9DZ1krJG_rI2AoFR2frBQAum9FBx013aS1YbS1smPQdXwYOBl137ML9PmZu6xDHX80oSTt1ZLcrNOjitqpfzPBPah9_KW4ED0XvAI-HQEp_lxNLmp2eTS-HsbENSsiCWct6dnW6-N_0kNcU6jrVZXoZS9BbkD6rBrrhXMy9mUYAmqzUh2tVL-tVJuVtejD32u8lPzxjj0Bt6ad3g</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Ke, Yunbo</creator><creator>Oskolkova, Olga V</creator><creator>Sarich, Nicolene</creator><creator>Tian, Yufeng</creator><creator>Sitikov, Albert</creator><creator>Tulapurkar, Mohan E</creator><creator>Son, Sophia</creator><creator>Birukova, Anna A</creator><creator>Birukov, Konstantin G</creator><general>American Physiological Society</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>7QP</scope><scope>7TS</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20171001</creationdate><title>Effects of prostaglandin lipid mediators on agonist-induced lung endothelial permeability and inflammation</title><author>Ke, Yunbo ; Oskolkova, Olga V ; Sarich, Nicolene ; Tian, Yufeng ; Sitikov, Albert ; Tulapurkar, Mohan E ; Son, Sophia ; Birukova, Anna A ; Birukov, Konstantin G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c496t-6e2acb7f34695454510e22675df9600a8467072e7daae324f9730775bb51ca883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adhesion tests</topic><topic>Animals</topic><topic>Arachidonic acid</topic><topic>Attenuation</topic><topic>Bacteria</topic><topic>Biological effects</topic><topic>Cell Membrane Permeability - drug effects</topic><topic>Contractility</topic><topic>Cytokines</topic><topic>Effects</topic><topic>Endothelial cells</topic><topic>Endothelium</topic><topic>Endothelium, Vascular - cytology</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - metabolism</topic><topic>Hemostatics - adverse effects</topic><topic>Humans</topic><topic>Hypersensitivity</topic><topic>In vivo methods and tests</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - pathology</topic><topic>Inflammatory response</topic><topic>Injury analysis</topic><topic>Intercellular adhesion molecule 1</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - metabolism</topic><topic>Lipids</topic><topic>Lipopolysaccharides</topic><topic>Lipopolysaccharides - adverse effects</topic><topic>Lung Injury - chemically induced</topic><topic>Lung Injury - drug therapy</topic><topic>Lung Injury - pathology</topic><topic>Lungs</topic><topic>Membrane permeability</topic><topic>Mice</topic><topic>Permeability</topic><topic>Prostacyclin</topic><topic>Prostaglandin E2</topic><topic>Prostaglandin endoperoxide synthase</topic><topic>Prostaglandins</topic><topic>Prostaglandins - pharmacology</topic><topic>Thrombin</topic><topic>Thrombin - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ke, Yunbo</creatorcontrib><creatorcontrib>Oskolkova, Olga V</creatorcontrib><creatorcontrib>Sarich, Nicolene</creatorcontrib><creatorcontrib>Tian, Yufeng</creatorcontrib><creatorcontrib>Sitikov, Albert</creatorcontrib><creatorcontrib>Tulapurkar, Mohan E</creatorcontrib><creatorcontrib>Son, Sophia</creatorcontrib><creatorcontrib>Birukova, Anna A</creatorcontrib><creatorcontrib>Birukov, Konstantin G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ke, Yunbo</au><au>Oskolkova, Olga V</au><au>Sarich, Nicolene</au><au>Tian, Yufeng</au><au>Sitikov, Albert</au><au>Tulapurkar, Mohan E</au><au>Son, Sophia</au><au>Birukova, Anna A</au><au>Birukov, Konstantin G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of prostaglandin lipid mediators on agonist-induced lung endothelial permeability and inflammation</atitle><jtitle>American journal of physiology. Lung cellular and molecular physiology</jtitle><addtitle>Am J Physiol Lung Cell Mol Physiol</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>313</volume><issue>4</issue><spage>L710</spage><epage>L721</epage><pages>L710-L721</pages><issn>1040-0605</issn><eissn>1522-1504</eissn><abstract>Prostaglandins (PG), the products of cyclooxygenase-mediated conversion of arachidonic acid, become upregulated in many situations including allergic response, inflammation, and injury, and exhibit a variety of biological activities. Previous studies described barrier-enhancing and anti-inflammatory effects of PGE
and PGI
on vascular endothelial cells (EC). Yet, the effects of other PG members on EC barrier and inflammatory activation have not been systematically analyzed. This study compared effects of PGE
, PGI
, PGF
, PGA
, PGJ
, and PGD
on human pulmonary EC. EC permeability was assessed by measurements of transendothelial electrical resistance and cell monolayer permeability for FITC-labeled tracer. Anti-inflammatory effects of PGs were evaluated by analysis of expression of adhesion molecule ICAM1 and secretion of soluble ICAM1 and cytokines by EC. PGE
, PGI
, and PGA
exhibited the most potent barrier-enhancing effects and most efficient attenuation of thrombin-induced EC permeability and contractile response, whereas PGI
effectively suppressed thrombin-induced permeability but was less efficient in the attenuation of prolonged EC hyperpermeability caused by interleukin-6 or bacterial wall lipopolysaccharide, LPS. PGD
showed a modest protective effect on the EC inflammatory response, whereas PGF
and PGJ
were without effect on agonist-induced EC barrier dysfunction. In vivo, PGE
, PGI
, and PGA
attenuated LPS-induced lung inflammation, whereas PGF
and PGJ
were without effect. Interestingly, PGD
exhibited a protective effect in the in vivo model of LPS-induced lung injury. This study provides a comprehensive analysis of barrier-protective and anti-inflammatory effects of different prostaglandins on lung EC in vitro and in vivo and identifies PGE
, PGI
, and PGA
as prostaglandins with the most potent protective properties.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>28663336</pmid><doi>10.1152/ajplung.00519.2016</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | American journal of physiology. Lung cellular and molecular physiology, 2017-10, Vol.313 (4), p.L710-L721 |
| issn | 1040-0605 1522-1504 |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adhesion tests Animals Arachidonic acid Attenuation Bacteria Biological effects Cell Membrane Permeability - drug effects Contractility Cytokines Effects Endothelial cells Endothelium Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Hemostatics - adverse effects Humans Hypersensitivity In vivo methods and tests Inflammation Inflammation - chemically induced Inflammation - drug therapy Inflammation - pathology Inflammatory response Injury analysis Intercellular adhesion molecule 1 Intercellular Adhesion Molecule-1 - metabolism Interleukin 6 Interleukin-6 - metabolism Lipids Lipopolysaccharides Lipopolysaccharides - adverse effects Lung Injury - chemically induced Lung Injury - drug therapy Lung Injury - pathology Lungs Membrane permeability Mice Permeability Prostacyclin Prostaglandin E2 Prostaglandin endoperoxide synthase Prostaglandins Prostaglandins - pharmacology Thrombin Thrombin - adverse effects |
| title | Effects of prostaglandin lipid mediators on agonist-induced lung endothelial permeability and inflammation |
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