Platelet‐activating factor increases mucosal permeability in rat intestine via tyrosine phosphorylation of E‐cadherin
Platelet‐activating factor (PAF), an inflammatory mediator, plays an important role in mediating intestinal injury. However, it remains unclear whether PAF has a function in the intestine. The production of PAF by normal intestine and by unstimulated intestinal epithelial cell lines suggests that PA...
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| creator | Tan, Xiao‐Di Chang, Hong Qu, Xiao‐Wu Caplan, Michael Gonzalez‐Crussi, Frank Hsueh, Wei |
| description | Platelet‐activating factor (PAF), an inflammatory mediator, plays an important role in mediating intestinal injury. However, it remains unclear whether PAF has a function in the intestine. The production of PAF by normal intestine and by unstimulated intestinal epithelial cell lines suggests that PAF may have a regulatory function in the normal bowel.
In this study we investigated the role of PAF in modulating intestinal mucosal permeability in rats. Lumen‐to‐blood transit of FD‐4 (dextran 4400), (an index of intestinal permeability), was assessed in sham‐operated rats and rats injected with PAF (1.25 μg kg−1, i.v., a dose insufficient to induce intestinal injury).
PAF‐induced villus cytoskeletal changes were examined by staining the intestine for F‐actin. The effect of PAF on tyrosine phosphorylation of the junctional protein E‐cadherin was examined by immunoprecipitation. Some rats were pretreated with AG1288 (a tyrosine kinase inhibitor) before PAF injection, and mucosal permeability change was assessed.
To investigate the role of endogenous PAF upon mucosal permeability, we studied the effect of PAF antagonists on (intraluminal) glucose‐induced increase in mucosal permeability.
We found that low dose PAF: (a) alters the cytoskeletal structure of intestinal epithelium, (b) causes the influx of FD4 from intestinal lumen to systemic circulation, (c) induces tyrosine phosphorylation of E‐cadherin and cadherin‐associated proteins. Glucose‐induced mucosal permeability increase is abolished by using two structurally different PAF antagonists.
These results suggest that endogenous PAF modulates macromolecular movement across the intestinal mucosal barrier, probably via tyrosine phosphorylation of E‐cadherin and cytoskeletal alteration of enterocytes.
British Journal of Pharmacology (2000) 129, 1522–1529; doi:10.1038/sj.bjp.0702939 |
| doi_str_mv | 10.1038/sj.bjp.0702939 |
| format | Article |
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In this study we investigated the role of PAF in modulating intestinal mucosal permeability in rats. Lumen‐to‐blood transit of FD‐4 (dextran 4400), (an index of intestinal permeability), was assessed in sham‐operated rats and rats injected with PAF (1.25 μg kg−1, i.v., a dose insufficient to induce intestinal injury).
PAF‐induced villus cytoskeletal changes were examined by staining the intestine for F‐actin. The effect of PAF on tyrosine phosphorylation of the junctional protein E‐cadherin was examined by immunoprecipitation. Some rats were pretreated with AG1288 (a tyrosine kinase inhibitor) before PAF injection, and mucosal permeability change was assessed.
To investigate the role of endogenous PAF upon mucosal permeability, we studied the effect of PAF antagonists on (intraluminal) glucose‐induced increase in mucosal permeability.
We found that low dose PAF: (a) alters the cytoskeletal structure of intestinal epithelium, (b) causes the influx of FD4 from intestinal lumen to systemic circulation, (c) induces tyrosine phosphorylation of E‐cadherin and cadherin‐associated proteins. Glucose‐induced mucosal permeability increase is abolished by using two structurally different PAF antagonists.
These results suggest that endogenous PAF modulates macromolecular movement across the intestinal mucosal barrier, probably via tyrosine phosphorylation of E‐cadherin and cytoskeletal alteration of enterocytes.
British Journal of Pharmacology (2000) 129, 1522–1529; doi:10.1038/sj.bjp.0702939</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1038/sj.bjp.0702939</identifier><identifier>PMID: 10742310</identifier><identifier>CODEN: BJPCBM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Azepines - pharmacology ; Biological and medical sciences ; Cadherins - chemistry ; Cadherins - metabolism ; Cell physiology ; Cytoskeleton - drug effects ; Cytoskeleton - metabolism ; Dextrans - blood ; Dextrans - pharmacokinetics ; Enzyme Inhibitors - pharmacology ; Epithelium - drug effects ; Epithelium - metabolism ; E‐cadherin ; Fundamental and applied biological sciences. Psychology ; Glucose - pharmacology ; Hypotension - chemically induced ; Intestinal Mucosa - drug effects ; Intestinal Mucosa - physiology ; intestinal permeability ; Intestines - drug effects ; Intestines - metabolism ; Leukocytosis - chemically induced ; Male ; Molecular and cellular biology ; Permeability - drug effects ; Phosphorylation ; Phosphotyrosine ; Platelet Activating Factor - adverse effects ; Platelet Activating Factor - pharmacology ; Platelet Activating Factor - physiology ; Platelet‐activating factor ; protein tyrosine phosphorylation ; Protein-Tyrosine Kinases - antagonists & inhibitors ; Quinolinium Compounds - pharmacology ; Rats ; Rats, Sprague-Dawley ; Responses to growth factors, tumor promotors, other factors ; small intestine ; Triazoles - pharmacology ; Tyrosine - metabolism ; Tyrphostins - pharmacology</subject><ispartof>British journal of pharmacology, 2000-04, Vol.129 (7), p.1522-1529</ispartof><rights>2000 British Pharmacological Society</rights><rights>2000 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Apr 2000</rights><rights>Copyright 2000, Nature Publishing Group 2000 Nature Publishing Group</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4861-f17eda0d3c24a8baf121a2fdb35d443456fd55cf3c957d3794b562e65af1ee0e3</citedby><cites>FETCH-LOGICAL-c4861-f17eda0d3c24a8baf121a2fdb35d443456fd55cf3c957d3794b562e65af1ee0e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571959/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1571959/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27903,27904,45553,45554,46387,46811,53769,53771</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1309880$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10742310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tan, Xiao‐Di</creatorcontrib><creatorcontrib>Chang, Hong</creatorcontrib><creatorcontrib>Qu, Xiao‐Wu</creatorcontrib><creatorcontrib>Caplan, Michael</creatorcontrib><creatorcontrib>Gonzalez‐Crussi, Frank</creatorcontrib><creatorcontrib>Hsueh, Wei</creatorcontrib><title>Platelet‐activating factor increases mucosal permeability in rat intestine via tyrosine phosphorylation of E‐cadherin</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Platelet‐activating factor (PAF), an inflammatory mediator, plays an important role in mediating intestinal injury. However, it remains unclear whether PAF has a function in the intestine. The production of PAF by normal intestine and by unstimulated intestinal epithelial cell lines suggests that PAF may have a regulatory function in the normal bowel.
In this study we investigated the role of PAF in modulating intestinal mucosal permeability in rats. Lumen‐to‐blood transit of FD‐4 (dextran 4400), (an index of intestinal permeability), was assessed in sham‐operated rats and rats injected with PAF (1.25 μg kg−1, i.v., a dose insufficient to induce intestinal injury).
PAF‐induced villus cytoskeletal changes were examined by staining the intestine for F‐actin. The effect of PAF on tyrosine phosphorylation of the junctional protein E‐cadherin was examined by immunoprecipitation. Some rats were pretreated with AG1288 (a tyrosine kinase inhibitor) before PAF injection, and mucosal permeability change was assessed.
To investigate the role of endogenous PAF upon mucosal permeability, we studied the effect of PAF antagonists on (intraluminal) glucose‐induced increase in mucosal permeability.
We found that low dose PAF: (a) alters the cytoskeletal structure of intestinal epithelium, (b) causes the influx of FD4 from intestinal lumen to systemic circulation, (c) induces tyrosine phosphorylation of E‐cadherin and cadherin‐associated proteins. Glucose‐induced mucosal permeability increase is abolished by using two structurally different PAF antagonists.
These results suggest that endogenous PAF modulates macromolecular movement across the intestinal mucosal barrier, probably via tyrosine phosphorylation of E‐cadherin and cytoskeletal alteration of enterocytes.
British Journal of Pharmacology (2000) 129, 1522–1529; doi:10.1038/sj.bjp.0702939</description><subject>Animals</subject><subject>Azepines - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cadherins - chemistry</subject><subject>Cadherins - metabolism</subject><subject>Cell physiology</subject><subject>Cytoskeleton - drug effects</subject><subject>Cytoskeleton - metabolism</subject><subject>Dextrans - blood</subject><subject>Dextrans - pharmacokinetics</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Epithelium - drug effects</subject><subject>Epithelium - metabolism</subject><subject>E‐cadherin</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glucose - pharmacology</subject><subject>Hypotension - chemically induced</subject><subject>Intestinal Mucosa - drug effects</subject><subject>Intestinal Mucosa - physiology</subject><subject>intestinal permeability</subject><subject>Intestines - drug effects</subject><subject>Intestines - metabolism</subject><subject>Leukocytosis - chemically induced</subject><subject>Male</subject><subject>Molecular and cellular biology</subject><subject>Permeability - drug effects</subject><subject>Phosphorylation</subject><subject>Phosphotyrosine</subject><subject>Platelet Activating Factor - adverse effects</subject><subject>Platelet Activating Factor - pharmacology</subject><subject>Platelet Activating Factor - physiology</subject><subject>Platelet‐activating factor</subject><subject>protein tyrosine phosphorylation</subject><subject>Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Quinolinium Compounds - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Responses to growth factors, tumor promotors, other factors</subject><subject>small intestine</subject><subject>Triazoles - pharmacology</subject><subject>Tyrosine - metabolism</subject><subject>Tyrphostins - pharmacology</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkcFu1DAQhi0EokvhyhFFiGsWTxzHyQWJVoUiVaIHOFsTZ9x1lI2DnV2UG4_AM_ZJ6tWuoJw4WOPRfDP_jH7GXgNfAxf1-9iv235ac8WLRjRP2ApKVeVS1PCUrTjnKgeo6zP2Isae81RU8jk7A67KQgBfseV2wJkGmu9__UYzuz3ObrzLbPr7kLnRBMJIMdvujI84ZBOFLWHrBjcvqZwFnFOYKaY2yvYOs3kJPh6SaeNjemFJCs6PmbfZVVIx2G0ouPEle2ZxiPTqFM_Z909X3y6v85uvn79cfrzJTVlXkFtQ1CHvhClKrFu0UAAWtmuF7MpSlLKynZTGCtNI1QnVlK2sCqpkIok4iXP24Th32rVb6gyNc8BBT8FtMSzao9P_Vka30Xd-r0EqaGSTBrw9DQj-xy5dqnu_C2PaWRegQKkGZILWR8ik62Mg-0cAuD44pWOvk1P65FRqePN4rUf40ZoEvDsBGA0ONuBoXPzLCd7U9QETR-ynG2j5j6q-uL0WVQPiAWwbs2g</recordid><startdate>200004</startdate><enddate>200004</enddate><creator>Tan, Xiao‐Di</creator><creator>Chang, Hong</creator><creator>Qu, Xiao‐Wu</creator><creator>Caplan, Michael</creator><creator>Gonzalez‐Crussi, Frank</creator><creator>Hsueh, Wei</creator><general>Blackwell Publishing Ltd</general><general>Nature Publishing</general><scope>IQODW</scope><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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>200004</creationdate><title>Platelet‐activating factor increases mucosal permeability in rat intestine via tyrosine phosphorylation of E‐cadherin</title><author>Tan, Xiao‐Di ; Chang, Hong ; Qu, Xiao‐Wu ; Caplan, Michael ; Gonzalez‐Crussi, Frank ; Hsueh, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4861-f17eda0d3c24a8baf121a2fdb35d443456fd55cf3c957d3794b562e65af1ee0e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Azepines - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cadherins - chemistry</topic><topic>Cadherins - metabolism</topic><topic>Cell physiology</topic><topic>Cytoskeleton - drug effects</topic><topic>Cytoskeleton - metabolism</topic><topic>Dextrans - blood</topic><topic>Dextrans - pharmacokinetics</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Epithelium - drug effects</topic><topic>Epithelium - metabolism</topic><topic>E‐cadherin</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glucose - pharmacology</topic><topic>Hypotension - chemically induced</topic><topic>Intestinal Mucosa - drug effects</topic><topic>Intestinal Mucosa - physiology</topic><topic>intestinal permeability</topic><topic>Intestines - drug effects</topic><topic>Intestines - metabolism</topic><topic>Leukocytosis - chemically induced</topic><topic>Male</topic><topic>Molecular and cellular biology</topic><topic>Permeability - drug effects</topic><topic>Phosphorylation</topic><topic>Phosphotyrosine</topic><topic>Platelet Activating Factor - adverse effects</topic><topic>Platelet Activating Factor - pharmacology</topic><topic>Platelet Activating Factor - physiology</topic><topic>Platelet‐activating factor</topic><topic>protein tyrosine phosphorylation</topic><topic>Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Quinolinium Compounds - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Responses to growth factors, tumor promotors, other factors</topic><topic>small intestine</topic><topic>Triazoles - pharmacology</topic><topic>Tyrosine - metabolism</topic><topic>Tyrphostins - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tan, Xiao‐Di</creatorcontrib><creatorcontrib>Chang, Hong</creatorcontrib><creatorcontrib>Qu, Xiao‐Wu</creatorcontrib><creatorcontrib>Caplan, Michael</creatorcontrib><creatorcontrib>Gonzalez‐Crussi, Frank</creatorcontrib><creatorcontrib>Hsueh, Wei</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences 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>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science 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 Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tan, Xiao‐Di</au><au>Chang, Hong</au><au>Qu, Xiao‐Wu</au><au>Caplan, Michael</au><au>Gonzalez‐Crussi, Frank</au><au>Hsueh, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Platelet‐activating factor increases mucosal permeability in rat intestine via tyrosine phosphorylation of E‐cadherin</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2000-04</date><risdate>2000</risdate><volume>129</volume><issue>7</issue><spage>1522</spage><epage>1529</epage><pages>1522-1529</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><coden>BJPCBM</coden><abstract>Platelet‐activating factor (PAF), an inflammatory mediator, plays an important role in mediating intestinal injury. However, it remains unclear whether PAF has a function in the intestine. The production of PAF by normal intestine and by unstimulated intestinal epithelial cell lines suggests that PAF may have a regulatory function in the normal bowel.
In this study we investigated the role of PAF in modulating intestinal mucosal permeability in rats. Lumen‐to‐blood transit of FD‐4 (dextran 4400), (an index of intestinal permeability), was assessed in sham‐operated rats and rats injected with PAF (1.25 μg kg−1, i.v., a dose insufficient to induce intestinal injury).
PAF‐induced villus cytoskeletal changes were examined by staining the intestine for F‐actin. The effect of PAF on tyrosine phosphorylation of the junctional protein E‐cadherin was examined by immunoprecipitation. Some rats were pretreated with AG1288 (a tyrosine kinase inhibitor) before PAF injection, and mucosal permeability change was assessed.
To investigate the role of endogenous PAF upon mucosal permeability, we studied the effect of PAF antagonists on (intraluminal) glucose‐induced increase in mucosal permeability.
We found that low dose PAF: (a) alters the cytoskeletal structure of intestinal epithelium, (b) causes the influx of FD4 from intestinal lumen to systemic circulation, (c) induces tyrosine phosphorylation of E‐cadherin and cadherin‐associated proteins. Glucose‐induced mucosal permeability increase is abolished by using two structurally different PAF antagonists.
These results suggest that endogenous PAF modulates macromolecular movement across the intestinal mucosal barrier, probably via tyrosine phosphorylation of E‐cadherin and cytoskeletal alteration of enterocytes.
British Journal of Pharmacology (2000) 129, 1522–1529; doi:10.1038/sj.bjp.0702939</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>10742310</pmid><doi>10.1038/sj.bjp.0702939</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete; Wiley Online Library Free Content; EZB-FREE-00999 freely available EZB journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Azepines - pharmacology Biological and medical sciences Cadherins - chemistry Cadherins - metabolism Cell physiology Cytoskeleton - drug effects Cytoskeleton - metabolism Dextrans - blood Dextrans - pharmacokinetics Enzyme Inhibitors - pharmacology Epithelium - drug effects Epithelium - metabolism E‐cadherin Fundamental and applied biological sciences. Psychology Glucose - pharmacology Hypotension - chemically induced Intestinal Mucosa - drug effects Intestinal Mucosa - physiology intestinal permeability Intestines - drug effects Intestines - metabolism Leukocytosis - chemically induced Male Molecular and cellular biology Permeability - drug effects Phosphorylation Phosphotyrosine Platelet Activating Factor - adverse effects Platelet Activating Factor - pharmacology Platelet Activating Factor - physiology Platelet‐activating factor protein tyrosine phosphorylation Protein-Tyrosine Kinases - antagonists & inhibitors Quinolinium Compounds - pharmacology Rats Rats, Sprague-Dawley Responses to growth factors, tumor promotors, other factors small intestine Triazoles - pharmacology Tyrosine - metabolism Tyrphostins - pharmacology |
| title | Platelet‐activating factor increases mucosal permeability in rat intestine via tyrosine phosphorylation of E‐cadherin |
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