Patent Ductus Arteriosus and Neonatal Death in Prostaglandin Receptor EP4-Deficient Mice
The physiological role of the prostaglandin E2receptor EP4 subtype was investigated by generation of EP4-deficient mice by gene targeting. Loss of the EP4 receptor was not lethalin utero,but most EP4 (−/−) neonates became pale and lethargic approximately 24 h after birth and died within 72 h. Less t...
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| Veröffentlicht in: | Biochemical and biophysical research communications 1998-05, Vol.246 (1), p.7-12 |
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| creator | Segi, Eri Sugimoto, Yukihiko Yamasaki, Atsushi Aze, Yoshiya Oida, Hiroji Nishimura, Tatsuya Murata, Takahiko Matsuoka, Toshiyuki Ushikubi, Fumitaka Hirose, Masaya Tanaka, Takashi Yoshida, Nobuaki Narumiya, Shuh Ichikawa, Atsushi |
| description | The physiological role of the prostaglandin E2receptor EP4 subtype was investigated by generation of EP4-deficient mice by gene targeting. Loss of the EP4 receptor was not lethalin utero,but most EP4 (−/−) neonates became pale and lethargic approximately 24 h after birth and died within 72 h. Less than 5% of the EP4 (−/−) mice survived and grew normally more than a year. Histological examination revealed that the ductus arteriosus in dead neonates remained open, while it was partially closed in the survivors.In situhybridization study showed that EP4 mRNA was strongly expressed in the ductus. These results suggest that neonatal death is at least partly due to patent ductus arteriosus and that the EP4 receptor plays a role in regulation of the patency of this vessel. They also indicate that normal function of the EP4 receptor is essential in neonatal adaptation of the circulatory system. |
| doi_str_mv | 10.1006/bbrc.1998.8461 |
| format | Article |
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Loss of the EP4 receptor was not lethalin utero,but most EP4 (−/−) neonates became pale and lethargic approximately 24 h after birth and died within 72 h. Less than 5% of the EP4 (−/−) mice survived and grew normally more than a year. Histological examination revealed that the ductus arteriosus in dead neonates remained open, while it was partially closed in the survivors.In situhybridization study showed that EP4 mRNA was strongly expressed in the ductus. These results suggest that neonatal death is at least partly due to patent ductus arteriosus and that the EP4 receptor plays a role in regulation of the patency of this vessel. They also indicate that normal function of the EP4 receptor is essential in neonatal adaptation of the circulatory system.</description><identifier>ISSN: 0006-291X</identifier><identifier>EISSN: 1090-2104</identifier><identifier>DOI: 10.1006/bbrc.1998.8461</identifier><identifier>PMID: 9600059</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Animals, Newborn ; Base Sequence ; Dinoprostone - physiology ; DNA Primers - genetics ; Ductus Arteriosus - pathology ; Ductus Arteriosus, Patent - etiology ; Ductus Arteriosus, Patent - genetics ; Ductus Arteriosus, Patent - physiopathology ; Female ; Gene Expression ; In Situ Hybridization ; Lung - pathology ; Male ; Mice ; Mice, Knockout ; Polymerase Chain Reaction ; Receptors, Prostaglandin E - deficiency ; Receptors, Prostaglandin E - genetics ; Receptors, Prostaglandin E - physiology ; Receptors, Prostaglandin E, EP4 Subtype ; RNA, Messenger - genetics ; RNA, Messenger - metabolism</subject><ispartof>Biochemical and biophysical research communications, 1998-05, Vol.246 (1), p.7-12</ispartof><rights>1998 Academic Press</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c405t-e2473b0e54ed565d4e4bbfb612bed419b0d11dd38a938cc4a21809dae897ed473</citedby><cites>FETCH-LOGICAL-c405t-e2473b0e54ed565d4e4bbfb612bed419b0d11dd38a938cc4a21809dae897ed473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/bbrc.1998.8461$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9600059$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Segi, Eri</creatorcontrib><creatorcontrib>Sugimoto, Yukihiko</creatorcontrib><creatorcontrib>Yamasaki, Atsushi</creatorcontrib><creatorcontrib>Aze, Yoshiya</creatorcontrib><creatorcontrib>Oida, Hiroji</creatorcontrib><creatorcontrib>Nishimura, Tatsuya</creatorcontrib><creatorcontrib>Murata, Takahiko</creatorcontrib><creatorcontrib>Matsuoka, Toshiyuki</creatorcontrib><creatorcontrib>Ushikubi, Fumitaka</creatorcontrib><creatorcontrib>Hirose, Masaya</creatorcontrib><creatorcontrib>Tanaka, Takashi</creatorcontrib><creatorcontrib>Yoshida, Nobuaki</creatorcontrib><creatorcontrib>Narumiya, Shuh</creatorcontrib><creatorcontrib>Ichikawa, Atsushi</creatorcontrib><title>Patent Ductus Arteriosus and Neonatal Death in Prostaglandin Receptor EP4-Deficient Mice</title><title>Biochemical and biophysical research communications</title><addtitle>Biochem Biophys Res Commun</addtitle><description>The physiological role of the prostaglandin E2receptor EP4 subtype was investigated by generation of EP4-deficient mice by gene targeting. Loss of the EP4 receptor was not lethalin utero,but most EP4 (−/−) neonates became pale and lethargic approximately 24 h after birth and died within 72 h. Less than 5% of the EP4 (−/−) mice survived and grew normally more than a year. Histological examination revealed that the ductus arteriosus in dead neonates remained open, while it was partially closed in the survivors.In situhybridization study showed that EP4 mRNA was strongly expressed in the ductus. These results suggest that neonatal death is at least partly due to patent ductus arteriosus and that the EP4 receptor plays a role in regulation of the patency of this vessel. They also indicate that normal function of the EP4 receptor is essential in neonatal adaptation of the circulatory system.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Base Sequence</subject><subject>Dinoprostone - physiology</subject><subject>DNA Primers - genetics</subject><subject>Ductus Arteriosus - pathology</subject><subject>Ductus Arteriosus, Patent - etiology</subject><subject>Ductus Arteriosus, Patent - genetics</subject><subject>Ductus Arteriosus, Patent - physiopathology</subject><subject>Female</subject><subject>Gene Expression</subject><subject>In Situ Hybridization</subject><subject>Lung - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Polymerase Chain Reaction</subject><subject>Receptors, Prostaglandin E - deficiency</subject><subject>Receptors, Prostaglandin E - genetics</subject><subject>Receptors, Prostaglandin E - physiology</subject><subject>Receptors, Prostaglandin E, EP4 Subtype</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><issn>0006-291X</issn><issn>1090-2104</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEtPwzAQhC0EKqVw5YaUE7cEO3ES-1i15SEVqBBIvVl-bMAobYrtIPHvcdSKGyevNd-OdgahS4IzgnF1o5TTGeGcZYxW5AiNCeY4zQmmx2iMI5HmnKxP0Zn3nxgTQis-QiNeRankY7ReyQDbkMx7HXqfTF0AZzsfR7k1yRN0Wxlkm8xBho_EbpOV63yQ721U4-8FNOxC55LFiqZzaKy2g9mj1XCOThrZerg4vBP0drt4nd2ny-e7h9l0mWqKy5BCTutCYSgpmLIqDQWqVKMqkiswlHCFDSHGFEzygmlNZU4Y5kYC43UE6mKCrve-O9d99eCD2FivoY0XQtd7UXPGq5oWEcz2oI4RvING7JzdSPcjCBZDlWKoUgxViqHKuHB1cO7VBswffugu6myvQ4z3bcEJP8TXYKwDHYTp7H_Wv0Frgwg</recordid><startdate>19980508</startdate><enddate>19980508</enddate><creator>Segi, Eri</creator><creator>Sugimoto, Yukihiko</creator><creator>Yamasaki, Atsushi</creator><creator>Aze, Yoshiya</creator><creator>Oida, Hiroji</creator><creator>Nishimura, Tatsuya</creator><creator>Murata, Takahiko</creator><creator>Matsuoka, Toshiyuki</creator><creator>Ushikubi, Fumitaka</creator><creator>Hirose, Masaya</creator><creator>Tanaka, Takashi</creator><creator>Yoshida, Nobuaki</creator><creator>Narumiya, Shuh</creator><creator>Ichikawa, Atsushi</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>19980508</creationdate><title>Patent Ductus Arteriosus and Neonatal Death in Prostaglandin Receptor EP4-Deficient Mice</title><author>Segi, Eri ; Sugimoto, Yukihiko ; Yamasaki, Atsushi ; Aze, Yoshiya ; Oida, Hiroji ; Nishimura, Tatsuya ; Murata, Takahiko ; Matsuoka, Toshiyuki ; Ushikubi, Fumitaka ; Hirose, Masaya ; Tanaka, Takashi ; Yoshida, Nobuaki ; Narumiya, Shuh ; Ichikawa, Atsushi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c405t-e2473b0e54ed565d4e4bbfb612bed419b0d11dd38a938cc4a21809dae897ed473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Base Sequence</topic><topic>Dinoprostone - physiology</topic><topic>DNA Primers - genetics</topic><topic>Ductus Arteriosus - pathology</topic><topic>Ductus Arteriosus, Patent - etiology</topic><topic>Ductus Arteriosus, Patent - genetics</topic><topic>Ductus Arteriosus, Patent - physiopathology</topic><topic>Female</topic><topic>Gene Expression</topic><topic>In Situ Hybridization</topic><topic>Lung - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Polymerase Chain Reaction</topic><topic>Receptors, Prostaglandin E - deficiency</topic><topic>Receptors, Prostaglandin E - genetics</topic><topic>Receptors, Prostaglandin E - physiology</topic><topic>Receptors, Prostaglandin E, EP4 Subtype</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Segi, Eri</creatorcontrib><creatorcontrib>Sugimoto, Yukihiko</creatorcontrib><creatorcontrib>Yamasaki, Atsushi</creatorcontrib><creatorcontrib>Aze, Yoshiya</creatorcontrib><creatorcontrib>Oida, Hiroji</creatorcontrib><creatorcontrib>Nishimura, Tatsuya</creatorcontrib><creatorcontrib>Murata, Takahiko</creatorcontrib><creatorcontrib>Matsuoka, Toshiyuki</creatorcontrib><creatorcontrib>Ushikubi, Fumitaka</creatorcontrib><creatorcontrib>Hirose, Masaya</creatorcontrib><creatorcontrib>Tanaka, Takashi</creatorcontrib><creatorcontrib>Yoshida, Nobuaki</creatorcontrib><creatorcontrib>Narumiya, Shuh</creatorcontrib><creatorcontrib>Ichikawa, Atsushi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biochemical and biophysical research communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Segi, Eri</au><au>Sugimoto, Yukihiko</au><au>Yamasaki, Atsushi</au><au>Aze, Yoshiya</au><au>Oida, Hiroji</au><au>Nishimura, Tatsuya</au><au>Murata, Takahiko</au><au>Matsuoka, Toshiyuki</au><au>Ushikubi, Fumitaka</au><au>Hirose, Masaya</au><au>Tanaka, Takashi</au><au>Yoshida, Nobuaki</au><au>Narumiya, Shuh</au><au>Ichikawa, Atsushi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Patent Ductus Arteriosus and Neonatal Death in Prostaglandin Receptor EP4-Deficient Mice</atitle><jtitle>Biochemical and biophysical research communications</jtitle><addtitle>Biochem Biophys Res Commun</addtitle><date>1998-05-08</date><risdate>1998</risdate><volume>246</volume><issue>1</issue><spage>7</spage><epage>12</epage><pages>7-12</pages><issn>0006-291X</issn><eissn>1090-2104</eissn><abstract>The physiological role of the prostaglandin E2receptor EP4 subtype was investigated by generation of EP4-deficient mice by gene targeting. Loss of the EP4 receptor was not lethalin utero,but most EP4 (−/−) neonates became pale and lethargic approximately 24 h after birth and died within 72 h. Less than 5% of the EP4 (−/−) mice survived and grew normally more than a year. Histological examination revealed that the ductus arteriosus in dead neonates remained open, while it was partially closed in the survivors.In situhybridization study showed that EP4 mRNA was strongly expressed in the ductus. These results suggest that neonatal death is at least partly due to patent ductus arteriosus and that the EP4 receptor plays a role in regulation of the patency of this vessel. They also indicate that normal function of the EP4 receptor is essential in neonatal adaptation of the circulatory system.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>9600059</pmid><doi>10.1006/bbrc.1998.8461</doi><tpages>6</tpages></addata></record> |
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| ispartof | Biochemical and biophysical research communications, 1998-05, Vol.246 (1), p.7-12 |
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| source | MEDLINE; ScienceDirect Journals (5 years ago - present) |
| subjects | Animals Animals, Newborn Base Sequence Dinoprostone - physiology DNA Primers - genetics Ductus Arteriosus - pathology Ductus Arteriosus, Patent - etiology Ductus Arteriosus, Patent - genetics Ductus Arteriosus, Patent - physiopathology Female Gene Expression In Situ Hybridization Lung - pathology Male Mice Mice, Knockout Polymerase Chain Reaction Receptors, Prostaglandin E - deficiency Receptors, Prostaglandin E - genetics Receptors, Prostaglandin E - physiology Receptors, Prostaglandin E, EP4 Subtype RNA, Messenger - genetics RNA, Messenger - metabolism |
| title | Patent Ductus Arteriosus and Neonatal Death in Prostaglandin Receptor EP4-Deficient Mice |
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