Increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or intrauterine growth retardation
Objective: This study was undertaken to determine whether preeclampsia and intrauterine growth retardation are associated with an increase in placental apoptosis. Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or intrauteri...
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| Veröffentlicht in: | American journal of obstetrics and gynecology 2002-01, Vol.186 (1), p.158-166 |
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| creator | Ishihara, Naonori Matsuo, Hiroya Murakoshi, Homare Laoag-Fernandez, Jovelle B. Samoto, Takashi Maruo, Takeshi |
| description | Objective: This study was undertaken to determine whether preeclampsia and intrauterine growth retardation are associated with an increase in placental apoptosis. Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or intrauterine growth retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. Results: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or intrauterine growth retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and intrauterine growth retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P |
| doi_str_mv | 10.1067/mob.2002.119176 |
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Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or intrauterine growth retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. Results: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or intrauterine growth retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and intrauterine growth retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P <.001; intrauterine growth retardation, P <.01). Transmission electron microscopy revealed the appearance of apoptotic nuclei in trophoblasts in severe preeclamptic term placenta. Conclusion: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and intrauterine growth retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.(Am J Obstet Gynecol 2002;186:158-66.)</description><identifier>ISSN: 0002-9378</identifier><identifier>EISSN: 1097-6868</identifier><identifier>DOI: 10.1067/mob.2002.119176</identifier><identifier>PMID: 11810103</identifier><identifier>CODEN: AJOGAH</identifier><language>eng</language><publisher>Philadelphia, PA: Elsevier Inc</publisher><subject>Apoptosis ; Bcl-2 protein ; Biological and medical sciences ; Diseases of mother, fetus and pregnancy ; fas Receptor - metabolism ; Female ; Fetal Growth Retardation - physiopathology ; Giant Cells - physiology ; Gynecology. Andrology. Obstetrics ; Humans ; Immunohistochemistry ; intrauterine growth retardation ; Medical sciences ; Microscopy, Electron ; placenta ; Placenta - physiopathology ; Placenta - ultrastructure ; Pre-Eclampsia - physiopathology ; preeclampsia ; Pregnancy ; Pregnancy. Fetus. Placenta ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Reference Values ; Trophoblasts - physiology</subject><ispartof>American journal of obstetrics and gynecology, 2002-01, Vol.186 (1), p.158-166</ispartof><rights>2002 Mosby, Inc.</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c439t-302847906e002508d40bef55cdc74cb5f7959d6f6822a262ac2130946af288343</citedby><cites>FETCH-LOGICAL-c439t-302847906e002508d40bef55cdc74cb5f7959d6f6822a262ac2130946af288343</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0002937802988587$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,4010,27900,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13464041$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11810103$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ishihara, Naonori</creatorcontrib><creatorcontrib>Matsuo, Hiroya</creatorcontrib><creatorcontrib>Murakoshi, Homare</creatorcontrib><creatorcontrib>Laoag-Fernandez, Jovelle B.</creatorcontrib><creatorcontrib>Samoto, Takashi</creatorcontrib><creatorcontrib>Maruo, Takeshi</creatorcontrib><title>Increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or intrauterine growth retardation</title><title>American journal of obstetrics and gynecology</title><addtitle>Am J Obstet Gynecol</addtitle><description>Objective: This study was undertaken to determine whether preeclampsia and intrauterine growth retardation are associated with an increase in placental apoptosis. Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or intrauterine growth retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. Results: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or intrauterine growth retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and intrauterine growth retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P <.001; intrauterine growth retardation, P <.01). Transmission electron microscopy revealed the appearance of apoptotic nuclei in trophoblasts in severe preeclamptic term placenta. Conclusion: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and intrauterine growth retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.(Am J Obstet Gynecol 2002;186:158-66.)</description><subject>Apoptosis</subject><subject>Bcl-2 protein</subject><subject>Biological and medical sciences</subject><subject>Diseases of mother, fetus and pregnancy</subject><subject>fas Receptor - metabolism</subject><subject>Female</subject><subject>Fetal Growth Retardation - physiopathology</subject><subject>Giant Cells - physiology</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>intrauterine growth retardation</subject><subject>Medical sciences</subject><subject>Microscopy, Electron</subject><subject>placenta</subject><subject>Placenta - physiopathology</subject><subject>Placenta - ultrastructure</subject><subject>Pre-Eclampsia - physiopathology</subject><subject>preeclampsia</subject><subject>Pregnancy</subject><subject>Pregnancy. Fetus. Placenta</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Reference Values</subject><subject>Trophoblasts - physiology</subject><issn>0002-9378</issn><issn>1097-6868</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kUGPFCEQhYnRuLOrZ2-Gi956Fmiabo5ms-omm3jRM6mmqx1MNyDQmvkP_miZzCR72hMh9b1H8R4h7zjbc6b62zWMe8GY2HOuea9ekB1num_UoIaXZMfqpNFtP1yR65x_na5Ci9fkivOBM87aHfn34G1CyDhRiCGWkF2mztNyQJqP3h6LCyWFeAjjArmcRodthQpgWmlcwKIvkKkNa1ychVKNxiNFVw0SjQnRLrDG7ICGVNUlwValziP9mcLfcqAJC6QJ6jv-DXk1w5Lx7eW8IT8-33-_-9o8fvvycPfpsbGy1aVpmRhkr5nC-qGODZNkI85dZyfbSzt2c687PalZDUKAUAKs4C3TUsEshqGV7Q35ePaNKfzeMBezumxxWcBj2LLpuaxJcVXB2zNoU8g54Wxiciuko-HMnAowtQBzKsCcC6iK9xfrbVxxeuIviVfgwwWAbGGZE3jr8hPXSiWZ5JXTZw5rEH8cJpOtQ29xcgltMVNwzy7xH0ZXpHM</recordid><startdate>200201</startdate><enddate>200201</enddate><creator>Ishihara, Naonori</creator><creator>Matsuo, Hiroya</creator><creator>Murakoshi, Homare</creator><creator>Laoag-Fernandez, Jovelle B.</creator><creator>Samoto, Takashi</creator><creator>Maruo, Takeshi</creator><general>Elsevier Inc</general><general>Elsevier</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>7X8</scope></search><sort><creationdate>200201</creationdate><title>Increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or intrauterine growth retardation</title><author>Ishihara, Naonori ; Matsuo, Hiroya ; Murakoshi, Homare ; Laoag-Fernandez, Jovelle B. ; Samoto, Takashi ; Maruo, Takeshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c439t-302847906e002508d40bef55cdc74cb5f7959d6f6822a262ac2130946af288343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Apoptosis</topic><topic>Bcl-2 protein</topic><topic>Biological and medical sciences</topic><topic>Diseases of mother, fetus and pregnancy</topic><topic>fas Receptor - metabolism</topic><topic>Female</topic><topic>Fetal Growth Retardation - physiopathology</topic><topic>Giant Cells - physiology</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>intrauterine growth retardation</topic><topic>Medical sciences</topic><topic>Microscopy, Electron</topic><topic>placenta</topic><topic>Placenta - physiopathology</topic><topic>Placenta - ultrastructure</topic><topic>Pre-Eclampsia - physiopathology</topic><topic>preeclampsia</topic><topic>Pregnancy</topic><topic>Pregnancy. Fetus. Placenta</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Reference Values</topic><topic>Trophoblasts - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ishihara, Naonori</creatorcontrib><creatorcontrib>Matsuo, Hiroya</creatorcontrib><creatorcontrib>Murakoshi, Homare</creatorcontrib><creatorcontrib>Laoag-Fernandez, Jovelle B.</creatorcontrib><creatorcontrib>Samoto, Takashi</creatorcontrib><creatorcontrib>Maruo, Takeshi</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>MEDLINE - Academic</collection><jtitle>American journal of obstetrics and gynecology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ishihara, Naonori</au><au>Matsuo, Hiroya</au><au>Murakoshi, Homare</au><au>Laoag-Fernandez, Jovelle B.</au><au>Samoto, Takashi</au><au>Maruo, Takeshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or intrauterine growth retardation</atitle><jtitle>American journal of obstetrics and gynecology</jtitle><addtitle>Am J Obstet Gynecol</addtitle><date>2002-01</date><risdate>2002</risdate><volume>186</volume><issue>1</issue><spage>158</spage><epage>166</epage><pages>158-166</pages><issn>0002-9378</issn><eissn>1097-6868</eissn><coden>AJOGAH</coden><abstract>Objective: This study was undertaken to determine whether preeclampsia and intrauterine growth retardation are associated with an increase in placental apoptosis. Study Design: Tissue specimens from 7 normal term placentas and each of 7 term placentas complicated by severe preeclampsia or intrauterine growth retardation were analyzed. Fas antigen and Bcl-2 protein expression were examined by the avidin/biotin immunoperoxidase method, whereas apoptosis was assessed by the terminal deoxynucleotidyl transferase deoxy-UTP-nick end labeling (TUNEL) method and transmission electron microscopy. Results: Fas antigen was immunolocalized in syncytiotrophoblasts in all placentas examined. No changes in the intensity of Fas antigen immunostaining in syncytiotrophoblasts were apparent among those placentas. Bcl-2 protein was abundantly immunolocalized in syncytiotrophoblasts in normal term placentas, but least abundant in term placentas complicated by severe preeclampsia or intrauterine growth retardation. Apoptosis was apparent in the nuclei of both cytotrophoblasts and syncytiotrophoblasts. The apoptosis positive rate of syncytiotrophoblast nuclei in severe preeclamptic and intrauterine growth retardation term placentas was significantly higher than that in normal term placentas (severe preeclampsia, P <.001; intrauterine growth retardation, P <.01). Transmission electron microscopy revealed the appearance of apoptotic nuclei in trophoblasts in severe preeclamptic term placenta. Conclusion: Decreased expression of Bcl-2 protein in syncytiotrophoblasts in severe preeclamptic and intrauterine growth retardation placentas may result in the increase in apoptosis in syncytiotrophoblasts in those placentas.(Am J Obstet Gynecol 2002;186:158-66.)</abstract><cop>Philadelphia, PA</cop><pub>Elsevier Inc</pub><pmid>11810103</pmid><doi>10.1067/mob.2002.119176</doi><tpages>9</tpages></addata></record> |
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| subjects | Apoptosis Bcl-2 protein Biological and medical sciences Diseases of mother, fetus and pregnancy fas Receptor - metabolism Female Fetal Growth Retardation - physiopathology Giant Cells - physiology Gynecology. Andrology. Obstetrics Humans Immunohistochemistry intrauterine growth retardation Medical sciences Microscopy, Electron placenta Placenta - physiopathology Placenta - ultrastructure Pre-Eclampsia - physiopathology preeclampsia Pregnancy Pregnancy. Fetus. Placenta Proto-Oncogene Proteins c-bcl-2 - metabolism Reference Values Trophoblasts - physiology |
| title | Increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or intrauterine growth retardation |
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