Neonatal vascularization and oxygen tension regulate appropriate perinatal renal medulla/papilla maturation.
Identifieur interne : 001A59 ( Main/Exploration ); précédent : 001A58; suivant : 001A60Neonatal vascularization and oxygen tension regulate appropriate perinatal renal medulla/papilla maturation.
Auteurs : Yu Leng Phua [Australie] ; Thierry Gilbert [France] ; Alexander Combes [Australie] ; Lorine Wilkinson [Australie] ; Melissa H. Little [Australie]Source :
- The Journal of pathology [ 1096-9896 ] ; 2016.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes, Animaux, Animaux nouveau-nés, Biologie informatique, Facteur de croissance endothéliale vasculaire de type A (génétique), Facteur de croissance endothéliale vasculaire de type A (métabolisme), Génotype, Hypoxie foetale (anatomopathologie), Hypoxie foetale (génétique), Hypoxie foetale (métabolisme), Malformations urogénitales (anatomopathologie), Malformations urogénitales (génétique), Malformations urogénitales (métabolisme), Modèles animaux de maladie humaine, Médulla rénale (), Médulla rénale (anatomopathologie), Médulla rénale (métabolisme), Néovascularisation pathologique (génétique), Oxygène (métabolisme), Phénotype, Reflux vésico-urétéral (anatomopathologie), Reflux vésico-urétéral (génétique), Reflux vésico-urétéral (métabolisme), Récepteurs de la protéine morphogénique osseuse (génétique), Récepteurs de la protéine morphogénique osseuse (métabolisme), Régulation de l'expression des gènes au cours du développement, Souris knockout, Voie de signalisation Wnt (génétique), Âge gestationnel.
- MESH :
- anatomopathologie : Hypoxie foetale, Malformations urogénitales, Médulla rénale, Reflux vésico-urétéral.
- génétique : Facteur de croissance endothéliale vasculaire de type A, Hypoxie foetale, Malformations urogénitales, Néovascularisation pathologique, Reflux vésico-urétéral, Récepteurs de la protéine morphogénique osseuse, Voie de signalisation Wnt.
- métabolisme : Facteur de croissance endothéliale vasculaire de type A, Hypoxie foetale, Malformations urogénitales, Médulla rénale, Oxygène, Reflux vésico-urétéral, Récepteurs de la protéine morphogénique osseuse.
- Analyse de profil d'expression de gènes, Animaux, Animaux nouveau-nés, Biologie informatique, Génotype, Modèles animaux de maladie humaine, Médulla rénale, Phénotype, Régulation de l'expression des gènes au cours du développement, Souris knockout, Âge gestationnel.
English descriptors
- KwdEn :
- Animals, Animals, Newborn, Bone Morphogenetic Protein Receptors (genetics), Bone Morphogenetic Protein Receptors (metabolism), Computational Biology, Disease Models, Animal, Fetal Hypoxia (genetics), Fetal Hypoxia (metabolism), Fetal Hypoxia (pathology), Gene Expression Profiling, Gene Expression Regulation, Developmental, Genotype, Gestational Age, Kidney Medulla (blood supply), Kidney Medulla (metabolism), Kidney Medulla (pathology), Mice, Knockout, Neovascularization, Pathologic (genetics), Oxygen (metabolism), Phenotype, Urogenital Abnormalities (genetics), Urogenital Abnormalities (metabolism), Urogenital Abnormalities (pathology), Vascular Endothelial Growth Factor A (genetics), Vascular Endothelial Growth Factor A (metabolism), Vesico-Ureteral Reflux (genetics), Vesico-Ureteral Reflux (metabolism), Vesico-Ureteral Reflux (pathology), Wnt Signaling Pathway (genetics).
- MESH :
- chemical , genetics : Bone Morphogenetic Protein Receptors, Vascular Endothelial Growth Factor A.
- chemical , metabolism : Bone Morphogenetic Protein Receptors, Oxygen, Vascular Endothelial Growth Factor A.
- blood supply : Kidney Medulla.
- genetics : Fetal Hypoxia, Neovascularization, Pathologic, Urogenital Abnormalities, Vesico-Ureteral Reflux, Wnt Signaling Pathway.
- metabolism : Fetal Hypoxia, Kidney Medulla, Urogenital Abnormalities, Vesico-Ureteral Reflux.
- pathology : Fetal Hypoxia, Kidney Medulla, Urogenital Abnormalities, Vesico-Ureteral Reflux.
- Animals, Animals, Newborn, Computational Biology, Disease Models, Animal, Gene Expression Profiling, Gene Expression Regulation, Developmental, Genotype, Gestational Age, Mice, Knockout, Phenotype.
Abstract
Congenital medullary dysplasia with obstructive nephropathy is a common congenital disorder observed in paediatric patients and represents the foremost cause of renal failure. However, the molecular processes regulating normal papillary outgrowth during the postnatal period are unclear. In this study, transcriptional profiling of the renal medulla across postnatal development revealed enrichment of non-canonical Wnt signalling, vascular development, and planar cell polarity genes, all of which may contribute to perinatal medulla/papilla maturation. These pathways were investigated in a model of papillary hypoplasia with functional obstruction, the Crim1(KST264/KST264) transgenic mouse. Postnatal elongation of the renal papilla via convergent extension was unaffected in the Crim1(KST264/KST264) hypoplastic renal papilla. In contrast, these mice displayed a disorganized papillary vascular network, tissue hypoxia, and elevated Vegfa expression. In addition, we demonstrate the involvement of accompanying systemic hypoxia arising from placental insufficiency, in appropriate papillary maturation. In conclusion, this study highlights the requirement for normal vascular development in collecting duct patterning, development of appropriate nephron architecture, and perinatal papillary maturation, such that disturbances contribute to obstructive nephropathy.
DOI: 10.1002/path.4690
PubMed: 26800422
Affiliations:
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Animals, Newborn</term>
<term>Bone Morphogenetic Protein Receptors (genetics)</term>
<term>Bone Morphogenetic Protein Receptors (metabolism)</term>
<term>Computational Biology</term>
<term>Disease Models, Animal</term>
<term>Fetal Hypoxia (genetics)</term>
<term>Fetal Hypoxia (metabolism)</term>
<term>Fetal Hypoxia (pathology)</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation, Developmental</term>
<term>Genotype</term>
<term>Gestational Age</term>
<term>Kidney Medulla (blood supply)</term>
<term>Kidney Medulla (metabolism)</term>
<term>Kidney Medulla (pathology)</term>
<term>Mice, Knockout</term>
<term>Neovascularization, Pathologic (genetics)</term>
<term>Oxygen (metabolism)</term>
<term>Phenotype</term>
<term>Urogenital Abnormalities (genetics)</term>
<term>Urogenital Abnormalities (metabolism)</term>
<term>Urogenital Abnormalities (pathology)</term>
<term>Vascular Endothelial Growth Factor A (genetics)</term>
<term>Vascular Endothelial Growth Factor A (metabolism)</term>
<term>Vesico-Ureteral Reflux (genetics)</term>
<term>Vesico-Ureteral Reflux (metabolism)</term>
<term>Vesico-Ureteral Reflux (pathology)</term>
<term>Wnt Signaling Pathway (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Animaux</term>
<term>Animaux nouveau-nés</term>
<term>Biologie informatique</term>
<term>Facteur de croissance endothéliale vasculaire de type A (génétique)</term>
<term>Facteur de croissance endothéliale vasculaire de type A (métabolisme)</term>
<term>Génotype</term>
<term>Hypoxie foetale (anatomopathologie)</term>
<term>Hypoxie foetale (génétique)</term>
<term>Hypoxie foetale (métabolisme)</term>
<term>Malformations urogénitales (anatomopathologie)</term>
<term>Malformations urogénitales (génétique)</term>
<term>Malformations urogénitales (métabolisme)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Médulla rénale ()</term>
<term>Médulla rénale (anatomopathologie)</term>
<term>Médulla rénale (métabolisme)</term>
<term>Néovascularisation pathologique (génétique)</term>
<term>Oxygène (métabolisme)</term>
<term>Phénotype</term>
<term>Reflux vésico-urétéral (anatomopathologie)</term>
<term>Reflux vésico-urétéral (génétique)</term>
<term>Reflux vésico-urétéral (métabolisme)</term>
<term>Récepteurs de la protéine morphogénique osseuse (génétique)</term>
<term>Récepteurs de la protéine morphogénique osseuse (métabolisme)</term>
<term>Régulation de l'expression des gènes au cours du développement</term>
<term>Souris knockout</term>
<term>Voie de signalisation Wnt (génétique)</term>
<term>Âge gestationnel</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Bone Morphogenetic Protein Receptors</term>
<term>Vascular Endothelial Growth Factor A</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bone Morphogenetic Protein Receptors</term>
<term>Oxygen</term>
<term>Vascular Endothelial Growth Factor A</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hypoxie foetale</term>
<term>Malformations urogénitales</term>
<term>Médulla rénale</term>
<term>Reflux vésico-urétéral</term>
</keywords>
<keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Kidney Medulla</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Fetal Hypoxia</term>
<term>Neovascularization, Pathologic</term>
<term>Urogenital Abnormalities</term>
<term>Vesico-Ureteral Reflux</term>
<term>Wnt Signaling Pathway</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type A</term>
<term>Hypoxie foetale</term>
<term>Malformations urogénitales</term>
<term>Néovascularisation pathologique</term>
<term>Reflux vésico-urétéral</term>
<term>Récepteurs de la protéine morphogénique osseuse</term>
<term>Voie de signalisation Wnt</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Fetal Hypoxia</term>
<term>Kidney Medulla</term>
<term>Urogenital Abnormalities</term>
<term>Vesico-Ureteral Reflux</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteur de croissance endothéliale vasculaire de type A</term>
<term>Hypoxie foetale</term>
<term>Malformations urogénitales</term>
<term>Médulla rénale</term>
<term>Oxygène</term>
<term>Reflux vésico-urétéral</term>
<term>Récepteurs de la protéine morphogénique osseuse</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Fetal Hypoxia</term>
<term>Kidney Medulla</term>
<term>Urogenital Abnormalities</term>
<term>Vesico-Ureteral Reflux</term>
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<term>Animals, Newborn</term>
<term>Computational Biology</term>
<term>Disease Models, Animal</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation, Developmental</term>
<term>Genotype</term>
<term>Gestational Age</term>
<term>Mice, Knockout</term>
<term>Phenotype</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term>
<term>Animaux</term>
<term>Animaux nouveau-nés</term>
<term>Biologie informatique</term>
<term>Génotype</term>
<term>Modèles animaux de maladie humaine</term>
<term>Médulla rénale</term>
<term>Phénotype</term>
<term>Régulation de l'expression des gènes au cours du développement</term>
<term>Souris knockout</term>
<term>Âge gestationnel</term>
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<front><div type="abstract" xml:lang="en">Congenital medullary dysplasia with obstructive nephropathy is a common congenital disorder observed in paediatric patients and represents the foremost cause of renal failure. However, the molecular processes regulating normal papillary outgrowth during the postnatal period are unclear. In this study, transcriptional profiling of the renal medulla across postnatal development revealed enrichment of non-canonical Wnt signalling, vascular development, and planar cell polarity genes, all of which may contribute to perinatal medulla/papilla maturation. These pathways were investigated in a model of papillary hypoplasia with functional obstruction, the Crim1(KST264/KST264) transgenic mouse. Postnatal elongation of the renal papilla via convergent extension was unaffected in the Crim1(KST264/KST264) hypoplastic renal papilla. In contrast, these mice displayed a disorganized papillary vascular network, tissue hypoxia, and elevated Vegfa expression. In addition, we demonstrate the involvement of accompanying systemic hypoxia arising from placental insufficiency, in appropriate papillary maturation. In conclusion, this study highlights the requirement for normal vascular development in collecting duct patterning, development of appropriate nephron architecture, and perinatal papillary maturation, such that disturbances contribute to obstructive nephropathy.</div>
</front>
</TEI>
<affiliations><list><country><li>Australie</li>
<li>France</li>
</country>
<region><li>Midi-Pyrénées</li>
<li>Occitanie (région administrative)</li>
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<tree><country name="Australie"><noRegion><name sortKey="Phua, Yu Leng" sort="Phua, Yu Leng" uniqKey="Phua Y" first="Yu Leng" last="Phua">Yu Leng Phua</name>
</noRegion>
<name sortKey="Combes, Alexander" sort="Combes, Alexander" uniqKey="Combes A" first="Alexander" last="Combes">Alexander Combes</name>
<name sortKey="Little, Melissa H" sort="Little, Melissa H" uniqKey="Little M" first="Melissa H" last="Little">Melissa H. Little</name>
<name sortKey="Wilkinson, Lorine" sort="Wilkinson, Lorine" uniqKey="Wilkinson L" first="Lorine" last="Wilkinson">Lorine Wilkinson</name>
</country>
<country name="France"><region name="Occitanie (région administrative)"><name sortKey="Gilbert, Thierry" sort="Gilbert, Thierry" uniqKey="Gilbert T" first="Thierry" last="Gilbert">Thierry Gilbert</name>
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