Gender-specific effect of overexpression of sFlt-1 in pregnant mice on fetal programming of blood pressure in the offspring later in life
Objective The purpose of this study was to determine whether fetal programming of adult blood pressure is altered in a previously characterized mouse model of preeclampsia that was induced by sFlt-1. Study Design CD-1 mouse mothers at day 8 of gestation were injected with an adenovirus carrying Flt...
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Veröffentlicht in: | American journal of obstetrics and gynecology 2007-10, Vol.197 (4), p.418.e1-418.e5 |
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container_title | American journal of obstetrics and gynecology |
container_volume | 197 |
creator | Lu, Fangxian, MD Bytautiene, Egle, MD Tamayo, Esther Gamble, Phyllis Anderson, Garland D., MD Hankins, Gary D.V., MD Longo, Monica, MD, PhD Saade, George R., MD |
description | Objective The purpose of this study was to determine whether fetal programming of adult blood pressure is altered in a previously characterized mouse model of preeclampsia that was induced by sFlt-1. Study Design CD-1 mouse mothers at day 8 of gestation were injected with an adenovirus carrying Flt 1-3 (109 plaque-forming units) or with an adenovirus carrying mFc as control (109 plaque-forming units). The resulting pups were followed until 6 months of age, at which time blood pressure (BP) was recorded continuously for 6 days. The offspring weight was also recorded from weaning until adulthood. Results BP was significantly higher in the male offspring that were born to sFlt-1–treated mothers compared with the controls. Male offspring from sFlt-1–treated mothers were significantly smaller from weaning until adulthood. However, there were no significant differences in BP and postweaning weight in female offspring between the 2 groups. Conclusion Our findings highlight the role of the intrauterine environment in the developmental origin of adult disease. |
doi_str_mv | 10.1016/j.ajog.2007.06.064 |
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Study Design CD-1 mouse mothers at day 8 of gestation were injected with an adenovirus carrying Flt 1-3 (109 plaque-forming units) or with an adenovirus carrying mFc as control (109 plaque-forming units). The resulting pups were followed until 6 months of age, at which time blood pressure (BP) was recorded continuously for 6 days. The offspring weight was also recorded from weaning until adulthood. Results BP was significantly higher in the male offspring that were born to sFlt-1–treated mothers compared with the controls. Male offspring from sFlt-1–treated mothers were significantly smaller from weaning until adulthood. However, there were no significant differences in BP and postweaning weight in female offspring between the 2 groups. Conclusion Our findings highlight the role of the intrauterine environment in the developmental origin of adult disease.</description><identifier>ISSN: 0002-9378</identifier><identifier>EISSN: 1097-6868</identifier><identifier>DOI: 10.1016/j.ajog.2007.06.064</identifier><identifier>PMID: 17904985</identifier><language>eng</language><publisher>United States: Mosby, Inc</publisher><subject>Animals ; Animals, Newborn ; Birth Weight - genetics ; Birth Weight - physiology ; Blood Pressure - physiology ; CD-1 mice ; developmental origin ; Female ; Fetal Development - physiology ; fetal programming ; Male ; Mice ; Obstetrics and Gynecology ; preeclampsia ; Pregnancy ; Random Allocation ; Sex Factors ; sFlt-1 ; Telemetry ; Transfection ; Vascular Endothelial Growth Factor Receptor-1 - biosynthesis ; Vascular Endothelial Growth Factor Receptor-1 - genetics</subject><ispartof>American journal of obstetrics and gynecology, 2007-10, Vol.197 (4), p.418.e1-418.e5</ispartof><rights>Mosby, Inc.</rights><rights>2007 Mosby, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-73ab425f4fd025bc669658f4cf1ecc47a9302eeaaba074bfc2f6abbf8ce64dc3</citedby><cites>FETCH-LOGICAL-c475t-73ab425f4fd025bc669658f4cf1ecc47a9302eeaaba074bfc2f6abbf8ce64dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S000293780700840X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17904985$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Fangxian, MD</creatorcontrib><creatorcontrib>Bytautiene, Egle, MD</creatorcontrib><creatorcontrib>Tamayo, Esther</creatorcontrib><creatorcontrib>Gamble, Phyllis</creatorcontrib><creatorcontrib>Anderson, Garland D., MD</creatorcontrib><creatorcontrib>Hankins, Gary D.V., MD</creatorcontrib><creatorcontrib>Longo, Monica, MD, PhD</creatorcontrib><creatorcontrib>Saade, George R., MD</creatorcontrib><title>Gender-specific effect of overexpression of sFlt-1 in pregnant mice on fetal programming of blood pressure in the offspring later in life</title><title>American journal of obstetrics and gynecology</title><addtitle>Am J Obstet Gynecol</addtitle><description>Objective The purpose of this study was to determine whether fetal programming of adult blood pressure is altered in a previously characterized mouse model of preeclampsia that was induced by sFlt-1. Study Design CD-1 mouse mothers at day 8 of gestation were injected with an adenovirus carrying Flt 1-3 (109 plaque-forming units) or with an adenovirus carrying mFc as control (109 plaque-forming units). The resulting pups were followed until 6 months of age, at which time blood pressure (BP) was recorded continuously for 6 days. The offspring weight was also recorded from weaning until adulthood. Results BP was significantly higher in the male offspring that were born to sFlt-1–treated mothers compared with the controls. Male offspring from sFlt-1–treated mothers were significantly smaller from weaning until adulthood. However, there were no significant differences in BP and postweaning weight in female offspring between the 2 groups. Conclusion Our findings highlight the role of the intrauterine environment in the developmental origin of adult disease.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Birth Weight - genetics</subject><subject>Birth Weight - physiology</subject><subject>Blood Pressure - physiology</subject><subject>CD-1 mice</subject><subject>developmental origin</subject><subject>Female</subject><subject>Fetal Development - physiology</subject><subject>fetal programming</subject><subject>Male</subject><subject>Mice</subject><subject>Obstetrics and Gynecology</subject><subject>preeclampsia</subject><subject>Pregnancy</subject><subject>Random Allocation</subject><subject>Sex Factors</subject><subject>sFlt-1</subject><subject>Telemetry</subject><subject>Transfection</subject><subject>Vascular Endothelial Growth Factor Receptor-1 - biosynthesis</subject><subject>Vascular Endothelial Growth Factor Receptor-1 - genetics</subject><issn>0002-9378</issn><issn>1097-6868</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9ksGK1TAUhoMoznX0BVxIV-56PUnTtAURZHBGYcCFs3AX0vTkmpom16QdnEfwrU28FwQXwoGQP9_5OfkTQl5S2FOg4s28V3M47BlAtweRiz8iOwpDV4te9I_JDgBYPTRdf0GepTSXLRvYU3JBuwH40Lc78usG_YSxTkfU1lhdoTGo1yqYKtxjxJ_HiCnZ4IuSrt1a08r6KqsHr_xaLVZjlU8NrsplORyiWhbrD4UfXQhT9cdhi1j61m-ZNiYdY0GcWjEW2VmDz8kTo1zCF-f1ktxdf7i7-ljffr75dPX-tta8a9e6a9TIWWu4mYC1oxZiEG1vuDYUdUbU0ABDVGpU0PHRaGaEGkfTaxR80s0leX2yzbP-2DCtcrFJo3PKY9iSFH3TCNoMGWQnUMeQUkQj89CLig-Sgiz5y1mW_GXJX4LIxXPTq7P7Ni44_W05B56BtycA8xXvLUaZtEWvcbIx5y6nYP_v_-6fdu2st1q57_iAaQ5b9Dk8SWViEuSX8uTlA0AH0HP42vwGrI-vPQ</recordid><startdate>20071001</startdate><enddate>20071001</enddate><creator>Lu, Fangxian, MD</creator><creator>Bytautiene, Egle, MD</creator><creator>Tamayo, Esther</creator><creator>Gamble, Phyllis</creator><creator>Anderson, Garland D., MD</creator><creator>Hankins, Gary D.V., MD</creator><creator>Longo, Monica, MD, PhD</creator><creator>Saade, George R., MD</creator><general>Mosby, 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>20071001</creationdate><title>Gender-specific effect of overexpression of sFlt-1 in pregnant mice on fetal programming of blood pressure in the offspring later in life</title><author>Lu, Fangxian, MD ; Bytautiene, Egle, MD ; Tamayo, Esther ; Gamble, Phyllis ; Anderson, Garland D., MD ; Hankins, Gary D.V., MD ; Longo, Monica, MD, PhD ; Saade, George R., MD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-73ab425f4fd025bc669658f4cf1ecc47a9302eeaaba074bfc2f6abbf8ce64dc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Birth Weight - genetics</topic><topic>Birth Weight - physiology</topic><topic>Blood Pressure - physiology</topic><topic>CD-1 mice</topic><topic>developmental origin</topic><topic>Female</topic><topic>Fetal Development - physiology</topic><topic>fetal programming</topic><topic>Male</topic><topic>Mice</topic><topic>Obstetrics and Gynecology</topic><topic>preeclampsia</topic><topic>Pregnancy</topic><topic>Random Allocation</topic><topic>Sex Factors</topic><topic>sFlt-1</topic><topic>Telemetry</topic><topic>Transfection</topic><topic>Vascular Endothelial Growth Factor Receptor-1 - biosynthesis</topic><topic>Vascular Endothelial Growth Factor Receptor-1 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Fangxian, MD</creatorcontrib><creatorcontrib>Bytautiene, Egle, MD</creatorcontrib><creatorcontrib>Tamayo, Esther</creatorcontrib><creatorcontrib>Gamble, Phyllis</creatorcontrib><creatorcontrib>Anderson, Garland D., MD</creatorcontrib><creatorcontrib>Hankins, Gary D.V., MD</creatorcontrib><creatorcontrib>Longo, Monica, MD, PhD</creatorcontrib><creatorcontrib>Saade, George R., MD</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>American journal of obstetrics and gynecology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Fangxian, MD</au><au>Bytautiene, Egle, MD</au><au>Tamayo, Esther</au><au>Gamble, Phyllis</au><au>Anderson, Garland D., MD</au><au>Hankins, Gary D.V., MD</au><au>Longo, Monica, MD, PhD</au><au>Saade, George R., MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gender-specific effect of overexpression of sFlt-1 in pregnant mice on fetal programming of blood pressure in the offspring later in life</atitle><jtitle>American journal of obstetrics and gynecology</jtitle><addtitle>Am J Obstet Gynecol</addtitle><date>2007-10-01</date><risdate>2007</risdate><volume>197</volume><issue>4</issue><spage>418.e1</spage><epage>418.e5</epage><pages>418.e1-418.e5</pages><issn>0002-9378</issn><eissn>1097-6868</eissn><abstract>Objective The purpose of this study was to determine whether fetal programming of adult blood pressure is altered in a previously characterized mouse model of preeclampsia that was induced by sFlt-1. Study Design CD-1 mouse mothers at day 8 of gestation were injected with an adenovirus carrying Flt 1-3 (109 plaque-forming units) or with an adenovirus carrying mFc as control (109 plaque-forming units). The resulting pups were followed until 6 months of age, at which time blood pressure (BP) was recorded continuously for 6 days. The offspring weight was also recorded from weaning until adulthood. Results BP was significantly higher in the male offspring that were born to sFlt-1–treated mothers compared with the controls. Male offspring from sFlt-1–treated mothers were significantly smaller from weaning until adulthood. However, there were no significant differences in BP and postweaning weight in female offspring between the 2 groups. Conclusion Our findings highlight the role of the intrauterine environment in the developmental origin of adult disease.</abstract><cop>United States</cop><pub>Mosby, Inc</pub><pmid>17904985</pmid><doi>10.1016/j.ajog.2007.06.064</doi></addata></record> |
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subjects | Animals Animals, Newborn Birth Weight - genetics Birth Weight - physiology Blood Pressure - physiology CD-1 mice developmental origin Female Fetal Development - physiology fetal programming Male Mice Obstetrics and Gynecology preeclampsia Pregnancy Random Allocation Sex Factors sFlt-1 Telemetry Transfection Vascular Endothelial Growth Factor Receptor-1 - biosynthesis Vascular Endothelial Growth Factor Receptor-1 - genetics |
title | Gender-specific effect of overexpression of sFlt-1 in pregnant mice on fetal programming of blood pressure in the offspring later in life |
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