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SEMA3B but Not CUL1 as Marker for Pre-Eclampsia Progression
An imbalance between pro- and anti-angiogenic factors contributes to impaired trophoblast invasion during pregnancy, leading to failure of uterine spiral artery remodeling, blood vessel ischemia, and pre-eclampsia (PE). Anti-angiogenic semaphorin 3B (SEMA3B) and pro-angiogenic cullin 1 (CUL1) are ex...
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Published in: | The Malaysian journal of medical sciences 2019-01, Vol.26 (1), p.66-72 |
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description | An imbalance between pro- and anti-angiogenic factors contributes to impaired trophoblast invasion during pregnancy, leading to failure of uterine spiral artery remodeling, blood vessel ischemia, and pre-eclampsia (PE). Anti-angiogenic semaphorin 3B (SEMA3B) and pro-angiogenic cullin 1 (CUL1) are expressed in both the placenta and maternal blood. The present study investigated correlations between serum and placental SEMA3B as well as CUL1 levels in late-onset PE.
This cross-sectional study included 50 patients with late-onset (≥ 32 weeks gestation) PE. Maternal serum was obtained before delivery, and placentas were obtained immediately after delivery. SEMA3B and CUL1 levels were evaluated by ELISA. Results were statistically analysed by Spearman correlation test, with a
< 0.05 considered statistically significant.
While elevated serum SEMA3B levels significantly correlated with increased placental SEMA3B levels in late-onset PE (
= 0.620,
= 0.000), alteration of serum CUL1 levels did not correlate with alteration of placental CUL1.
Alteration of circulating maternal SEMA3B, but not CUL1, levels can potentially be used to monitor PE progression during pregnancy. |
doi_str_mv | 10.21315/mjms2019.26.1.6 |
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This cross-sectional study included 50 patients with late-onset (≥ 32 weeks gestation) PE. Maternal serum was obtained before delivery, and placentas were obtained immediately after delivery. SEMA3B and CUL1 levels were evaluated by ELISA. Results were statistically analysed by Spearman correlation test, with a
< 0.05 considered statistically significant.
While elevated serum SEMA3B levels significantly correlated with increased placental SEMA3B levels in late-onset PE (
= 0.620,
= 0.000), alteration of serum CUL1 levels did not correlate with alteration of placental CUL1.
Alteration of circulating maternal SEMA3B, but not CUL1, levels can potentially be used to monitor PE progression during pregnancy.</description><identifier>ISSN: 1394-195X</identifier><identifier>EISSN: 2180-4303</identifier><identifier>DOI: 10.21315/mjms2019.26.1.6</identifier><identifier>PMID: 30914894</identifier><language>eng</language><publisher>Malaysia: Universiti Sains Malaysia Press</publisher><subject>Blood pressure ; Cell cycle ; Cesarean section ; Enzymes ; Gestational age ; Hypertension ; Hypoxia ; Original ; Placenta ; Preeclampsia ; Pregnancy ; Proteins ; Signal transduction ; Statistical analysis ; Vagina</subject><ispartof>The Malaysian journal of medical sciences, 2019-01, Vol.26 (1), p.66-72</ispartof><rights>Copyright Universiti Sains Malaysia Press Jan/Feb 2019</rights><rights>Penerbit Universiti Sains Malaysia, 2019 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c424t-b49d6446163dee0332dc6d7dfe246edbe04848327573b44679a532d8b25f4d83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419870/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6419870/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4009,27902,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30914894$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Samara, Tjam Diana</creatorcontrib><creatorcontrib>Liem, Isabella Kurnia</creatorcontrib><creatorcontrib>Prijanti, Ani Retno</creatorcontrib><creatorcontrib>Andrijono</creatorcontrib><creatorcontrib>Doctoral Program in Biomedical Sciences, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</creatorcontrib><creatorcontrib>Department of Anatomy, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</creatorcontrib><creatorcontrib>Department of Biochemistry and Molecular Biology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</creatorcontrib><creatorcontrib>Department of Obstetrics and Gynecology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</creatorcontrib><creatorcontrib>Department of Anatomy, Faculty of Medicine, Trisakti University, Jakarta, Indonesia</creatorcontrib><title>SEMA3B but Not CUL1 as Marker for Pre-Eclampsia Progression</title><title>The Malaysian journal of medical sciences</title><addtitle>Malays J Med Sci</addtitle><description>An imbalance between pro- and anti-angiogenic factors contributes to impaired trophoblast invasion during pregnancy, leading to failure of uterine spiral artery remodeling, blood vessel ischemia, and pre-eclampsia (PE). Anti-angiogenic semaphorin 3B (SEMA3B) and pro-angiogenic cullin 1 (CUL1) are expressed in both the placenta and maternal blood. The present study investigated correlations between serum and placental SEMA3B as well as CUL1 levels in late-onset PE.
This cross-sectional study included 50 patients with late-onset (≥ 32 weeks gestation) PE. Maternal serum was obtained before delivery, and placentas were obtained immediately after delivery. SEMA3B and CUL1 levels were evaluated by ELISA. Results were statistically analysed by Spearman correlation test, with a
< 0.05 considered statistically significant.
While elevated serum SEMA3B levels significantly correlated with increased placental SEMA3B levels in late-onset PE (
= 0.620,
= 0.000), alteration of serum CUL1 levels did not correlate with alteration of placental CUL1.
Alteration of circulating maternal SEMA3B, but not CUL1, levels can potentially be used to monitor PE progression during pregnancy.</description><subject>Blood pressure</subject><subject>Cell cycle</subject><subject>Cesarean section</subject><subject>Enzymes</subject><subject>Gestational age</subject><subject>Hypertension</subject><subject>Hypoxia</subject><subject>Original</subject><subject>Placenta</subject><subject>Preeclampsia</subject><subject>Pregnancy</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Statistical analysis</subject><subject>Vagina</subject><issn>1394-195X</issn><issn>2180-4303</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><recordid>eNpdkUtLw0AUhQdRbK3uXUnAjZvEeSdBEGqpD2hVsIK7YZKZ1NQkU2cSwX_vaB-oq8vlfudwDweAYwQjjAhi5_WidhiiNMI8QhHfAX2MEhhSAsku6COS0hCl7KUHDpxbQEgY5sk-6BGYIpqktA8unsbTIbkKsq4N7k0bjJ4nKJAumEr7pm1QGBs8Wh2O80rWS1dKv5m51c6VpjkEe4WsnD5azwGYXY9no9tw8nBzNxpOwpxi2oYZTRWnlCNOlNaQEKxyrmJVaEy5VpmGNKEJwTGLSea5OJXMM0mGWUFVQgbgcmW77LJaq1w3rZWVWNqylvZTGFmKv5emfBVz8yE4RWkSQ29wtjaw5r3TrhV16XJdVbLRpnMCe4xxGEPs0dN_6MJ0tvHpBGaUMv-pjzEAcEXl1jhndbF9BkHxU4zYFCMwF0h8S05-h9gKNk2QL_i-h7M</recordid><startdate>201901</startdate><enddate>201901</enddate><creator>Samara, Tjam Diana</creator><creator>Liem, Isabella Kurnia</creator><creator>Prijanti, Ani Retno</creator><creator>Andrijono</creator><general>Universiti Sains Malaysia Press</general><general>Penerbit Universiti Sains Malaysia</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BVBZV</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201901</creationdate><title>SEMA3B but Not CUL1 as Marker for Pre-Eclampsia Progression</title><author>Samara, Tjam Diana ; Liem, Isabella Kurnia ; Prijanti, Ani Retno ; Andrijono</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c424t-b49d6446163dee0332dc6d7dfe246edbe04848327573b44679a532d8b25f4d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Blood pressure</topic><topic>Cell cycle</topic><topic>Cesarean section</topic><topic>Enzymes</topic><topic>Gestational age</topic><topic>Hypertension</topic><topic>Hypoxia</topic><topic>Original</topic><topic>Placenta</topic><topic>Preeclampsia</topic><topic>Pregnancy</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Statistical analysis</topic><topic>Vagina</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Samara, Tjam Diana</creatorcontrib><creatorcontrib>Liem, Isabella Kurnia</creatorcontrib><creatorcontrib>Prijanti, Ani Retno</creatorcontrib><creatorcontrib>Andrijono</creatorcontrib><creatorcontrib>Doctoral Program in Biomedical Sciences, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</creatorcontrib><creatorcontrib>Department of Anatomy, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</creatorcontrib><creatorcontrib>Department of Biochemistry and Molecular Biology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</creatorcontrib><creatorcontrib>Department of Obstetrics and Gynecology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</creatorcontrib><creatorcontrib>Department of Anatomy, Faculty of Medicine, Trisakti University, Jakarta, Indonesia</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>East & South Asia Database</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Malaysian journal of medical sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Samara, Tjam Diana</au><au>Liem, Isabella Kurnia</au><au>Prijanti, Ani Retno</au><au>Andrijono</au><aucorp>Doctoral Program in Biomedical Sciences, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</aucorp><aucorp>Department of Anatomy, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</aucorp><aucorp>Department of Biochemistry and Molecular Biology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</aucorp><aucorp>Department of Obstetrics and Gynecology, Faculty of Medicine, Universitas Indonesia, Jakarta, Indonesia</aucorp><aucorp>Department of Anatomy, Faculty of Medicine, Trisakti University, Jakarta, Indonesia</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SEMA3B but Not CUL1 as Marker for Pre-Eclampsia Progression</atitle><jtitle>The Malaysian journal of medical sciences</jtitle><addtitle>Malays J Med Sci</addtitle><date>2019-01</date><risdate>2019</risdate><volume>26</volume><issue>1</issue><spage>66</spage><epage>72</epage><pages>66-72</pages><issn>1394-195X</issn><eissn>2180-4303</eissn><abstract>An imbalance between pro- and anti-angiogenic factors contributes to impaired trophoblast invasion during pregnancy, leading to failure of uterine spiral artery remodeling, blood vessel ischemia, and pre-eclampsia (PE). Anti-angiogenic semaphorin 3B (SEMA3B) and pro-angiogenic cullin 1 (CUL1) are expressed in both the placenta and maternal blood. The present study investigated correlations between serum and placental SEMA3B as well as CUL1 levels in late-onset PE.
This cross-sectional study included 50 patients with late-onset (≥ 32 weeks gestation) PE. Maternal serum was obtained before delivery, and placentas were obtained immediately after delivery. SEMA3B and CUL1 levels were evaluated by ELISA. Results were statistically analysed by Spearman correlation test, with a
< 0.05 considered statistically significant.
While elevated serum SEMA3B levels significantly correlated with increased placental SEMA3B levels in late-onset PE (
= 0.620,
= 0.000), alteration of serum CUL1 levels did not correlate with alteration of placental CUL1.
Alteration of circulating maternal SEMA3B, but not CUL1, levels can potentially be used to monitor PE progression during pregnancy.</abstract><cop>Malaysia</cop><pub>Universiti Sains Malaysia Press</pub><pmid>30914894</pmid><doi>10.21315/mjms2019.26.1.6</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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language | eng |
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source | PubMed Central |
subjects | Blood pressure Cell cycle Cesarean section Enzymes Gestational age Hypertension Hypoxia Original Placenta Preeclampsia Pregnancy Proteins Signal transduction Statistical analysis Vagina |
title | SEMA3B but Not CUL1 as Marker for Pre-Eclampsia Progression |
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