Neonatal vascularization and oxygen tension regulate appropriate perinatal renal medulla/papilla maturation.
Identifieur interne : 002046 ( PubMed/Curation ); précédent : 002045; suivant : 002047Neonatal 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
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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></keywords><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></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><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></keywords></textClass></profileDesc></teiHeader><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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26800422</PMID><DateCreated><Year>2016</Year><Month>03</Month><Day>22</Day></DateCreated><DateCompleted><Year>2016</Year><Month>08</Month><Day>01</Day></DateCompleted><DateRevised><Year>2016</Year><Month>03</Month><Day>22</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1096-9896</ISSN><JournalIssue CitedMedium="Internet"><Volume>238</Volume><Issue>5</Issue><PubDate><Year>2016</Year><Month>Apr</Month></PubDate></JournalIssue><Title>The Journal of pathology</Title><ISOAbbreviation>J. Pathol.</ISOAbbreviation></Journal><ArticleTitle>Neonatal vascularization and oxygen tension regulate appropriate perinatal renal medulla/papilla maturation.</ArticleTitle><Pagination><MedlinePgn>665-76</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/path.4690</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Phua</LastName><ForeName>Yu Leng</ForeName><Initials>YL</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-3428-8669</Identifier><AffiliationInfo><Affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Rangos Research Center, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>School of Medicine, Department of Pediatrics, Division of Nephrology, University of Pittsburgh, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gilbert</LastName><ForeName>Thierry</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Centre for Developmental Biology, University Paul Sabatier, Toulouse, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Combes</LastName><ForeName>Alexander</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Anatomy and Neuroscience, University of Melbourne, Melbourne, VIC, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatrics, University of Melbourne, Melbourne, VIC, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wilkinson</LastName><ForeName>Lorine</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Little</LastName><ForeName>Melissa H</ForeName><Initials>MH</Initials><AffiliationInfo><Affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pediatrics, University of Melbourne, Melbourne, VIC, Australia.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Murdoch Children's Research Institute, Royal Children's Hospital, Melbourne, VIC, Australia.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Pathol</MedlineTA><NlmUniqueID>0204634</NlmUniqueID><ISSNLinking>0022-3417</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C518411">Crim1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467480">vascular endothelial growth factor A, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.30</RegistryNumber><NameOfSubstance UI="D052004">Bone Morphogenetic Protein Receptors</NameOfSubstance></Chemical><Chemical><RegistryNumber>S88TT14065</RegistryNumber><NameOfSubstance UI="D010100">Oxygen</NameOfSubstance></Chemical></ChemicalList><SupplMeshList><SupplMeshName Type="Disease" UI="C566906">Cakut</SupplMeshName></SupplMeshList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000831" MajorTopicYN="N">Animals, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D052004" MajorTopicYN="N">Bone Morphogenetic Protein Receptors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019295" MajorTopicYN="N">Computational Biology</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005311" MajorTopicYN="N">Fetal Hypoxia</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018507" MajorTopicYN="N">Gene Expression Regulation, Developmental</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005865" MajorTopicYN="N">Gestational Age</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007679" MajorTopicYN="N">Kidney Medulla</DescriptorName><QualifierName UI="Q000098" MajorTopicYN="Y">blood supply</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009389" MajorTopicYN="Y">Neovascularization, Pathologic</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010100" MajorTopicYN="N">Oxygen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014564" MajorTopicYN="N">Urogenital Abnormalities</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042461" MajorTopicYN="N">Vascular Endothelial Growth Factor A</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014718" MajorTopicYN="N">Vesico-Ureteral Reflux</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060449" MajorTopicYN="N">Wnt Signaling Pathway</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Crim1</Keyword><Keyword MajorTopicYN="N">convergent extension</Keyword><Keyword MajorTopicYN="N">hypoxia</Keyword><Keyword MajorTopicYN="N">medullary vasculature</Keyword><Keyword MajorTopicYN="N">non-canonical Wnt signalling</Keyword><Keyword MajorTopicYN="N">renal papilla</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>09</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>11</Month><Day>21</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>01</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>1</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>1</Month><Day>23</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>8</Month><Day>2</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26800422</ArticleId><ArticleId IdType="doi">10.1002/path.4690</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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