iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling
Calcium independent group VIA phospholipase A(2) (iPLA(2)β) is up-regulated in vascular smooth muscle cells in some diseases, but whether the up-regulated iPLA(2)β affects vascular morphology and blood pressure is unknown. The current study addresses this question by evaluating the basal- and angiot...
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| creator | Calderon, Lindsay E Liu, Shu Su, Wen Xie, Zhongwen Guo, Zhenheng Eberhard, Wanda Gong, Ming C |
| description | Calcium independent group VIA phospholipase A(2) (iPLA(2)β) is up-regulated in vascular smooth muscle cells in some diseases, but whether the up-regulated iPLA(2)β affects vascular morphology and blood pressure is unknown. The current study addresses this question by evaluating the basal- and angiotensin II infusion-induced vascular remodeling and hypertension in smooth muscle specific iPLA(2)β transgenic (iPLA(2)β-Tg) mice.
Blood pressure was monitored by radiotelemetry and vascular remodeling was assessed by morphologic analysis. We found that the angiotensin II-induced increase in diastolic pressure was significantly higher in iPLA(2)β-Tg than iPLA(2)β-Wt mice, whereas, the basal blood pressure was not significantly different. The media thickness and media∶lumen ratio of the mesenteric arteries were significantly increased in angiotensin II-infused iPLA(2)β-Tg mice. Analysis revealed no difference in vascular smooth muscle cell proliferation. In contrast, adenovirus-mediated iPLA(2)β overexpression in cultured vascular smooth muscle cells promoted angiotensin II-induced [(3)H]-leucine incorporation, indicating enhanced hypertrophy. Moreover, angiotensin II infusion-induced c-Jun phosphorylation in vascular smooth muscle cells overexpressing iPLA2β to higher levels, which was abolished by inhibition of 12/15 lipoxygenase. In addition, we found that angiotensin II up-regulated the endogenous iPLA(2)β protein in-vitro and in-vivo.
The present study reports that iPLA(2)β up-regulation exacerbates angiotensin II-induced vascular smooth muscle cell hypertrophy, vascular remodeling and hypertension via the 12/15 lipoxygenase and c-Jun pathways. |
| doi_str_mv | 10.1371/journal.pone.0031850 |
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Blood pressure was monitored by radiotelemetry and vascular remodeling was assessed by morphologic analysis. We found that the angiotensin II-induced increase in diastolic pressure was significantly higher in iPLA(2)β-Tg than iPLA(2)β-Wt mice, whereas, the basal blood pressure was not significantly different. The media thickness and media∶lumen ratio of the mesenteric arteries were significantly increased in angiotensin II-infused iPLA(2)β-Tg mice. Analysis revealed no difference in vascular smooth muscle cell proliferation. In contrast, adenovirus-mediated iPLA(2)β overexpression in cultured vascular smooth muscle cells promoted angiotensin II-induced [(3)H]-leucine incorporation, indicating enhanced hypertrophy. Moreover, angiotensin II infusion-induced c-Jun phosphorylation in vascular smooth muscle cells overexpressing iPLA2β to higher levels, which was abolished by inhibition of 12/15 lipoxygenase. In addition, we found that angiotensin II up-regulated the endogenous iPLA(2)β protein in-vitro and in-vivo.
The present study reports that iPLA(2)β up-regulation exacerbates angiotensin II-induced vascular smooth muscle cell hypertrophy, vascular remodeling and hypertension via the 12/15 lipoxygenase and c-Jun pathways.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0031850</identifier><identifier>PMID: 22363752</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Angiotensin ; Angiotensin II ; Angiotensin II - administration & dosage ; Angiotensin II - pharmacology ; Animals ; Aorta, Thoracic - drug effects ; Aorta, Thoracic - physiopathology ; Arachidonate 15-Lipoxygenase ; Arachidonic Acid - metabolism ; Arteries ; Biology ; Blood ; Blood pressure ; Blood Pressure - drug effects ; c-Jun protein ; Calcium ; Cell proliferation ; Cell Proliferation - drug effects ; Circulatory system ; Coronary vessels ; Diabetes ; Diastole - drug effects ; Diastolic pressure ; Group VI Phospholipases A2 - metabolism ; Hypertension ; Hypertension - enzymology ; Hypertension - pathology ; Hypertension - physiopathology ; Hypertrophy ; Internal medicine ; Ischemia ; Kinases ; Leucine ; Leucine - metabolism ; Lipoxygenase ; Medicine ; Mesenteric Arteries - drug effects ; Mesenteric Arteries - physiopathology ; Metabolites ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Muscle, Smooth, Vascular - drug effects ; Muscle, Smooth, Vascular - enzymology ; Muscle, Smooth, Vascular - pathology ; Muscle, Smooth, Vascular - physiopathology ; Myocytes, Smooth Muscle - drug effects ; Myocytes, Smooth Muscle - enzymology ; Myocytes, Smooth Muscle - pathology ; Organ Specificity - drug effects ; p38 Mitogen-Activated Protein Kinases - metabolism ; Phospholipase ; Phospholipase A2 ; Phosphorylation ; Physiology ; Proteins ; Proto-Oncogene Proteins c-jun - metabolism ; Rats ; Rodents ; Signal Transduction - drug effects ; Smooth muscle ; Transcription factors ; Transgenic mice</subject><ispartof>PloS one, 2012-02, Vol.7 (2), p.e31850-e31850</ispartof><rights>2012 Calderon et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Calderon et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-d946eb522846f42a501edc872b6ff13ab80495df51576f0ab7bd9a54a9de550d3</citedby><cites>FETCH-LOGICAL-c455t-d946eb522846f42a501edc872b6ff13ab80495df51576f0ab7bd9a54a9de550d3</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/PMC3282780/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3282780/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22363752$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Calderon, Lindsay E</creatorcontrib><creatorcontrib>Liu, Shu</creatorcontrib><creatorcontrib>Su, Wen</creatorcontrib><creatorcontrib>Xie, Zhongwen</creatorcontrib><creatorcontrib>Guo, Zhenheng</creatorcontrib><creatorcontrib>Eberhard, Wanda</creatorcontrib><creatorcontrib>Gong, Ming C</creatorcontrib><title>iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Calcium independent group VIA phospholipase A(2) (iPLA(2)β) is up-regulated in vascular smooth muscle cells in some diseases, but whether the up-regulated iPLA(2)β affects vascular morphology and blood pressure is unknown. The current study addresses this question by evaluating the basal- and angiotensin II infusion-induced vascular remodeling and hypertension in smooth muscle specific iPLA(2)β transgenic (iPLA(2)β-Tg) mice.
Blood pressure was monitored by radiotelemetry and vascular remodeling was assessed by morphologic analysis. We found that the angiotensin II-induced increase in diastolic pressure was significantly higher in iPLA(2)β-Tg than iPLA(2)β-Wt mice, whereas, the basal blood pressure was not significantly different. The media thickness and media∶lumen ratio of the mesenteric arteries were significantly increased in angiotensin II-infused iPLA(2)β-Tg mice. Analysis revealed no difference in vascular smooth muscle cell proliferation. In contrast, adenovirus-mediated iPLA(2)β overexpression in cultured vascular smooth muscle cells promoted angiotensin II-induced [(3)H]-leucine incorporation, indicating enhanced hypertrophy. Moreover, angiotensin II infusion-induced c-Jun phosphorylation in vascular smooth muscle cells overexpressing iPLA2β to higher levels, which was abolished by inhibition of 12/15 lipoxygenase. In addition, we found that angiotensin II up-regulated the endogenous iPLA(2)β protein in-vitro and in-vivo.
The present study reports that iPLA(2)β up-regulation exacerbates angiotensin II-induced vascular smooth muscle cell hypertrophy, vascular remodeling and hypertension via the 12/15 lipoxygenase and c-Jun pathways.</description><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - administration & dosage</subject><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Aorta, Thoracic - drug effects</subject><subject>Aorta, Thoracic - physiopathology</subject><subject>Arachidonate 15-Lipoxygenase</subject><subject>Arachidonic Acid - metabolism</subject><subject>Arteries</subject><subject>Biology</subject><subject>Blood</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>c-Jun protein</subject><subject>Calcium</subject><subject>Cell proliferation</subject><subject>Cell Proliferation - drug effects</subject><subject>Circulatory system</subject><subject>Coronary vessels</subject><subject>Diabetes</subject><subject>Diastole - drug effects</subject><subject>Diastolic pressure</subject><subject>Group VI Phospholipases A2 - metabolism</subject><subject>Hypertension</subject><subject>Hypertension - enzymology</subject><subject>Hypertension - pathology</subject><subject>Hypertension - physiopathology</subject><subject>Hypertrophy</subject><subject>Internal medicine</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Leucine</subject><subject>Leucine - metabolism</subject><subject>Lipoxygenase</subject><subject>Medicine</subject><subject>Mesenteric Arteries - drug effects</subject><subject>Mesenteric Arteries - physiopathology</subject><subject>Metabolites</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Muscle, Smooth, Vascular - drug effects</subject><subject>Muscle, Smooth, Vascular - enzymology</subject><subject>Muscle, Smooth, Vascular - pathology</subject><subject>Muscle, Smooth, Vascular - physiopathology</subject><subject>Myocytes, Smooth Muscle - drug effects</subject><subject>Myocytes, Smooth Muscle - enzymology</subject><subject>Myocytes, Smooth Muscle - pathology</subject><subject>Organ Specificity - drug effects</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Phospholipase</subject><subject>Phospholipase A2</subject><subject>Phosphorylation</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-jun - metabolism</subject><subject>Rats</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Smooth muscle</subject><subject>Transcription factors</subject><subject>Transgenic mice</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptkstu1DAUhiMEohd4AwSRWHSVwZfYiTdIVcVlpJFgAWvrJD6Z8Sixg52M2tfiQXgm3E5atYiNbR1_5_f5rT_L3lCyoryiH_Z-Dg761egdrgjhtBbkWXZKFWeFZIQ_f3Q-yc5i3BMieC3ly-yEMS55Jdhp5u33zSX78zv3Bwx4PQaM0XqXW5fHwftplw9zbHvM8RpaDA1MGHNwW-sndDFR63VhnZlbNPnuZsRwV04C4Ex-gNjOPYQ84OAN9tZtX2UvOugjvl728-zn508_rr4Wm29f1leXm6IthZgKo0qJjWCsLmVXMhCEomnrijWy6yiHpialEqYTVFSyI9BUjVEgSlAGhSCGn2fvjrpj76Ne_ipqyhmvRa04T8T6SBgPez0GO0C40R6sviv4sNUQJpu864YqRZVsCZRVSYE0FUpBsGMGGaQ1aX1cXpubIQ2KbgrQPxF9euPsTm_9QXNWs6omSeBiEQj-14xx0oONLfY9OPRz1IpxUalS0ES-_4f8v7nySLXBxxiwe5iFEn0bn_sufRsfvcQntb197OOh6T4v_C_aC8as</recordid><startdate>20120220</startdate><enddate>20120220</enddate><creator>Calderon, Lindsay E</creator><creator>Liu, Shu</creator><creator>Su, Wen</creator><creator>Xie, Zhongwen</creator><creator>Guo, Zhenheng</creator><creator>Eberhard, Wanda</creator><creator>Gong, Ming C</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20120220</creationdate><title>iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling</title><author>Calderon, Lindsay E ; Liu, Shu ; Su, Wen ; Xie, Zhongwen ; Guo, Zhenheng ; Eberhard, Wanda ; Gong, Ming C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-d946eb522846f42a501edc872b6ff13ab80495df51576f0ab7bd9a54a9de550d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - administration & dosage</topic><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Aorta, Thoracic - drug effects</topic><topic>Aorta, Thoracic - physiopathology</topic><topic>Arachidonate 15-Lipoxygenase</topic><topic>Arachidonic Acid - metabolism</topic><topic>Arteries</topic><topic>Biology</topic><topic>Blood</topic><topic>Blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>c-Jun protein</topic><topic>Calcium</topic><topic>Cell proliferation</topic><topic>Cell Proliferation - drug effects</topic><topic>Circulatory system</topic><topic>Coronary vessels</topic><topic>Diabetes</topic><topic>Diastole - drug effects</topic><topic>Diastolic pressure</topic><topic>Group VI Phospholipases A2 - metabolism</topic><topic>Hypertension</topic><topic>Hypertension - enzymology</topic><topic>Hypertension - pathology</topic><topic>Hypertension - physiopathology</topic><topic>Hypertrophy</topic><topic>Internal medicine</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Leucine</topic><topic>Leucine - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Calderon, Lindsay E</au><au>Liu, Shu</au><au>Su, Wen</au><au>Xie, Zhongwen</au><au>Guo, Zhenheng</au><au>Eberhard, Wanda</au><au>Gong, Ming C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-02-20</date><risdate>2012</risdate><volume>7</volume><issue>2</issue><spage>e31850</spage><epage>e31850</epage><pages>e31850-e31850</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Calcium independent group VIA phospholipase A(2) (iPLA(2)β) is up-regulated in vascular smooth muscle cells in some diseases, but whether the up-regulated iPLA(2)β affects vascular morphology and blood pressure is unknown. The current study addresses this question by evaluating the basal- and angiotensin II infusion-induced vascular remodeling and hypertension in smooth muscle specific iPLA(2)β transgenic (iPLA(2)β-Tg) mice.
Blood pressure was monitored by radiotelemetry and vascular remodeling was assessed by morphologic analysis. We found that the angiotensin II-induced increase in diastolic pressure was significantly higher in iPLA(2)β-Tg than iPLA(2)β-Wt mice, whereas, the basal blood pressure was not significantly different. The media thickness and media∶lumen ratio of the mesenteric arteries were significantly increased in angiotensin II-infused iPLA(2)β-Tg mice. Analysis revealed no difference in vascular smooth muscle cell proliferation. In contrast, adenovirus-mediated iPLA(2)β overexpression in cultured vascular smooth muscle cells promoted angiotensin II-induced [(3)H]-leucine incorporation, indicating enhanced hypertrophy. Moreover, angiotensin II infusion-induced c-Jun phosphorylation in vascular smooth muscle cells overexpressing iPLA2β to higher levels, which was abolished by inhibition of 12/15 lipoxygenase. In addition, we found that angiotensin II up-regulated the endogenous iPLA(2)β protein in-vitro and in-vivo.
The present study reports that iPLA(2)β up-regulation exacerbates angiotensin II-induced vascular smooth muscle cell hypertrophy, vascular remodeling and hypertension via the 12/15 lipoxygenase and c-Jun pathways.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22363752</pmid><doi>10.1371/journal.pone.0031850</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1323858933 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Angiotensin Angiotensin II Angiotensin II - administration & dosage Angiotensin II - pharmacology Animals Aorta, Thoracic - drug effects Aorta, Thoracic - physiopathology Arachidonate 15-Lipoxygenase Arachidonic Acid - metabolism Arteries Biology Blood Blood pressure Blood Pressure - drug effects c-Jun protein Calcium Cell proliferation Cell Proliferation - drug effects Circulatory system Coronary vessels Diabetes Diastole - drug effects Diastolic pressure Group VI Phospholipases A2 - metabolism Hypertension Hypertension - enzymology Hypertension - pathology Hypertension - physiopathology Hypertrophy Internal medicine Ischemia Kinases Leucine Leucine - metabolism Lipoxygenase Medicine Mesenteric Arteries - drug effects Mesenteric Arteries - physiopathology Metabolites Mice Mice, Inbred C57BL Mice, Transgenic Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - enzymology Muscle, Smooth, Vascular - pathology Muscle, Smooth, Vascular - physiopathology Myocytes, Smooth Muscle - drug effects Myocytes, Smooth Muscle - enzymology Myocytes, Smooth Muscle - pathology Organ Specificity - drug effects p38 Mitogen-Activated Protein Kinases - metabolism Phospholipase Phospholipase A2 Phosphorylation Physiology Proteins Proto-Oncogene Proteins c-jun - metabolism Rats Rodents Signal Transduction - drug effects Smooth muscle Transcription factors Transgenic mice |
| title | iPLA2β overexpression in smooth muscle exacerbates angiotensin II-induced hypertension and vascular remodeling |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-01T14%3A35%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=iPLA2%CE%B2%20overexpression%20in%20smooth%20muscle%20exacerbates%20angiotensin%20II-induced%20hypertension%20and%20vascular%20remodeling&rft.jtitle=PloS%20one&rft.au=Calderon,%20Lindsay%20E&rft.date=2012-02-20&rft.volume=7&rft.issue=2&rft.spage=e31850&rft.epage=e31850&rft.pages=e31850-e31850&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0031850&rft_dat=%3Cproquest_plos_%3E2936588191%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1323858933&rft_id=info:pmid/22363752&rft_doaj_id=oai_doaj_org_article_b199196c0a4741a0b7e650ef2de2af2d&rfr_iscdi=true |