FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2137065024> ?p ?o ?g. }

• W2137065024 endingPage "S243" @default.
• W2137065024 startingPage "S243" @default.
• W2137065024 abstract "ObjectiveApoptotic signaling pathways controlling the first week of embryonic development are poorly characterized. The objective of this study, is to understand mechanisms controlling the early embryonic development in term of survival and apoptotic signals.DesignHuman unfertilized MII oocytes, day 3 embryos and day 5/6 blastocysts were included after informed consent of the patients and authority approval. MII oocytes, day 1.5 embryos and day 3/4 blastocysts were collected from mice in vivo. We compared gene expression profiles between MII and day 3 embryos, MII and blastocyts, day 3 embryos and blastocyts in human as well as between MII and day1.5 embryos, MII and blastocysts, day 1.5 embryos and blastocysts in mouse.Materials and MethodsThe mRNAs extracted from each embryonic stage were analyzed on GeneChip Human Genome U133 Plus 2.0 or Mouse Genome 430 2.0 Arrays. Significant Analysis of Microarrays was used to identify genes differentially between groups.ResultsGene expression profiles between embryonic stages diverge in human compared with the mouse. Indeed, we identified 1801, 1031, 2023 over-expressed genes exclusive to the MII, day 3 embryos and blastocyst stage respectively in human versus 869, 3 and 299 genes in mouse. In addition, only 439 over-expressed genes were in common between embryonic stages in human versus 2439 genes in mouse. Consequently, survival signals differ between embryonic stages in human (over-expression of IGFBP1, HDGF2 in MII oocytes versus FGFR2 and IGFR1 in blastocysts) as for apoptotic signals (over-expression of CASP6 in oocytes versus CASP2 in blastocysts). Inversely, survival and apoptotic signals were stable between mouse embryonic stages. Moreover, signaling pathways related to oxidative stress, hypoxia and DNA damage were over-represented in the human.ConclusionThis study opens new perspectives for understanding the molecular regulation of oocyte and normal and degenerative embryo survival and death. ObjectiveApoptotic signaling pathways controlling the first week of embryonic development are poorly characterized. The objective of this study, is to understand mechanisms controlling the early embryonic development in term of survival and apoptotic signals. Apoptotic signaling pathways controlling the first week of embryonic development are poorly characterized. The objective of this study, is to understand mechanisms controlling the early embryonic development in term of survival and apoptotic signals. DesignHuman unfertilized MII oocytes, day 3 embryos and day 5/6 blastocysts were included after informed consent of the patients and authority approval. MII oocytes, day 1.5 embryos and day 3/4 blastocysts were collected from mice in vivo. We compared gene expression profiles between MII and day 3 embryos, MII and blastocyts, day 3 embryos and blastocyts in human as well as between MII and day1.5 embryos, MII and blastocysts, day 1.5 embryos and blastocysts in mouse. Human unfertilized MII oocytes, day 3 embryos and day 5/6 blastocysts were included after informed consent of the patients and authority approval. MII oocytes, day 1.5 embryos and day 3/4 blastocysts were collected from mice in vivo. We compared gene expression profiles between MII and day 3 embryos, MII and blastocyts, day 3 embryos and blastocyts in human as well as between MII and day1.5 embryos, MII and blastocysts, day 1.5 embryos and blastocysts in mouse. Materials and MethodsThe mRNAs extracted from each embryonic stage were analyzed on GeneChip Human Genome U133 Plus 2.0 or Mouse Genome 430 2.0 Arrays. Significant Analysis of Microarrays was used to identify genes differentially between groups. The mRNAs extracted from each embryonic stage were analyzed on GeneChip Human Genome U133 Plus 2.0 or Mouse Genome 430 2.0 Arrays. Significant Analysis of Microarrays was used to identify genes differentially between groups. ResultsGene expression profiles between embryonic stages diverge in human compared with the mouse. Indeed, we identified 1801, 1031, 2023 over-expressed genes exclusive to the MII, day 3 embryos and blastocyst stage respectively in human versus 869, 3 and 299 genes in mouse. In addition, only 439 over-expressed genes were in common between embryonic stages in human versus 2439 genes in mouse. Consequently, survival signals differ between embryonic stages in human (over-expression of IGFBP1, HDGF2 in MII oocytes versus FGFR2 and IGFR1 in blastocysts) as for apoptotic signals (over-expression of CASP6 in oocytes versus CASP2 in blastocysts). Inversely, survival and apoptotic signals were stable between mouse embryonic stages. Moreover, signaling pathways related to oxidative stress, hypoxia and DNA damage were over-represented in the human. Gene expression profiles between embryonic stages diverge in human compared with the mouse. Indeed, we identified 1801, 1031, 2023 over-expressed genes exclusive to the MII, day 3 embryos and blastocyst stage respectively in human versus 869, 3 and 299 genes in mouse. In addition, only 439 over-expressed genes were in common between embryonic stages in human versus 2439 genes in mouse. Consequently, survival signals differ between embryonic stages in human (over-expression of IGFBP1, HDGF2 in MII oocytes versus FGFR2 and IGFR1 in blastocysts) as for apoptotic signals (over-expression of CASP6 in oocytes versus CASP2 in blastocysts). Inversely, survival and apoptotic signals were stable between mouse embryonic stages. Moreover, signaling pathways related to oxidative stress, hypoxia and DNA damage were over-represented in the human. ConclusionThis study opens new perspectives for understanding the molecular regulation of oocyte and normal and degenerative embryo survival and death. This study opens new perspectives for understanding the molecular regulation of oocyte and normal and degenerative embryo survival and death." @default.
• W2137065024 created "2016-06-24" @default.
• W2137065024 creator A5014537968 @default.
• W2137065024 creator A5051689782 @default.
• W2137065024 creator A5065250369 @default.
• W2137065024 creator A5069011607 @default.
• W2137065024 creator A5073867025 @default.
• W2137065024 date "2013-09-01" @default.
• W2137065024 modified "2023-09-28" @default.
• W2137065024 title "Apoptotic signaling pathways during early embryonic development: comparison between human and mouse" @default.
• W2137065024 doi "https://doi.org/10.1016/j.fertnstert.2013.07.1228" @default.
• W2137065024 hasPublicationYear "2013" @default.
• W2137065024 type Work @default.
• W2137065024 sameAs 2137065024 @default.
• W2137065024 citedByCount "0" @default.
• W2137065024 crossrefType "journal-article" @default.
• W2137065024 hasAuthorship W2137065024A5014537968 @default.
• W2137065024 hasAuthorship W2137065024A5051689782 @default.
• W2137065024 hasAuthorship W2137065024A5065250369 @default.
• W2137065024 hasAuthorship W2137065024A5069011607 @default.
• W2137065024 hasAuthorship W2137065024A5073867025 @default.
• W2137065024 hasBestOaLocation W21370650241 @default.
• W2137065024 hasConcept C104317684 @default.
• W2137065024 hasConcept C145103041 @default.
• W2137065024 hasConcept C150194340 @default.
• W2137065024 hasConcept C16685009 @default.
• W2137065024 hasConcept C18431079 @default.
• W2137065024 hasConcept C186836561 @default.
• W2137065024 hasConcept C196843134 @default.
• W2137065024 hasConcept C2778177303 @default.
• W2137065024 hasConcept C54355233 @default.
• W2137065024 hasConcept C71924100 @default.
• W2137065024 hasConcept C8415881 @default.
• W2137065024 hasConcept C86803240 @default.
• W2137065024 hasConcept C87073359 @default.
• W2137065024 hasConcept C95444343 @default.
• W2137065024 hasConceptScore W2137065024C104317684 @default.
• W2137065024 hasConceptScore W2137065024C145103041 @default.
• W2137065024 hasConceptScore W2137065024C150194340 @default.
• W2137065024 hasConceptScore W2137065024C16685009 @default.
• W2137065024 hasConceptScore W2137065024C18431079 @default.
• W2137065024 hasConceptScore W2137065024C186836561 @default.
• W2137065024 hasConceptScore W2137065024C196843134 @default.
• W2137065024 hasConceptScore W2137065024C2778177303 @default.
• W2137065024 hasConceptScore W2137065024C54355233 @default.
• W2137065024 hasConceptScore W2137065024C71924100 @default.
• W2137065024 hasConceptScore W2137065024C8415881 @default.
• W2137065024 hasConceptScore W2137065024C86803240 @default.
• W2137065024 hasConceptScore W2137065024C87073359 @default.
• W2137065024 hasConceptScore W2137065024C95444343 @default.
• W2137065024 hasIssue "3" @default.
• W2137065024 hasLocation W21370650241 @default.
• W2137065024 hasOpenAccess W2137065024 @default.
• W2137065024 hasPrimaryLocation W21370650241 @default.
• W2137065024 hasRelatedWork W1973087247 @default.
• W2137065024 hasRelatedWork W1977107428 @default.
• W2137065024 hasRelatedWork W2038259893 @default.
• W2137065024 hasRelatedWork W2069673065 @default.
• W2137065024 hasRelatedWork W2170165366 @default.
• W2137065024 hasRelatedWork W2199361193 @default.
• W2137065024 hasRelatedWork W2223970316 @default.
• W2137065024 hasRelatedWork W2295731892 @default.
• W2137065024 hasRelatedWork W2359365475 @default.
• W2137065024 hasRelatedWork W2188570840 @default.
• W2137065024 hasVolume "100" @default.
• W2137065024 isParatext "false" @default.
• W2137065024 isRetracted "false" @default.
• W2137065024 magId "2137065024" @default.
• W2137065024 workType "article" @default.