Vascular Abnormalities in Mice Deficient for the G Protein-Coupled Receptor GPR4 That Functions as a pH Sensor

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Published inMolecular and Cellular Biology Vol. 27; no. 4; pp. 1334 - 1347
Main Authors Yang, Li V., Radu, Caius G., Roy, Meenakshi, Lee, Sunyoung, McLaughlin, Jami, Teitell, Michael A., Iruela-Arispe, M. Luisa, Witte, Owen N.
Format Journal Article
LanguageEnglish
Published United States American Society for Microbiology 01.02.2007
Taylor & Francis
Subjects
Animals
Animals, Newborn
Aorta - abnormalities
Blood Vessels - abnormalities
Blood Vessels - embryology
Cells, Cultured
Crosses, Genetic
Embryo, Mammalian - abnormalities
Embryo, Mammalian - blood supply
Embryo, Mammalian - pathology
Female
Gene Targeting
Genotype
Hemorrhage - congenital
Humans
Hydrogen-Ion Concentration
Litter Size
Lung - abnormalities
Lung - embryology
Lung - pathology
Male
Mesangial Cells - pathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Penetrance
Receptors, G-Protein-Coupled - deficiency
Receptors, G-Protein-Coupled - metabolism
Respiratory Tract Diseases - congenital
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Abstract Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
AbstractList GPR4 is a G protein-coupled receptor expressed in the vasculature, lung, kidney, and other tissues. In vitro ectopic overexpression studies implicated GPR4 in sensing extracellular pH changes leading to cyclic AMP (cAMP) production. To investigate its biological roles in vivo, we generated GPR4-deficient mice by homologous recombination. Whereas GPR4-null adult mice appeared phenotypically normal, neonates showed a higher frequency of perinatal mortality. The average litter size from GPR4 −/− intercrosses was ∼30% smaller than that from GPR4 +/+ intercrosses on N3 and N5 C57BL/6 genetic backgrounds. A fraction of knockout embryos and neonates had spontaneous hemorrhages, dilated and tortuous subcutaneous blood vessels, and defective vascular smooth muscle cell coverage. Mesangial cells in kidney glomeruli were also significantly reduced in GPR4-null neonates. Some neonates exhibited respiratory distress with airway lining cell metaplasia. To examine whether GPR4 is functionally involved in vascular pH sensing, an ex vivo aortic ring assay was used under defined pH conditions. Compared to wild-type aortas, microvessel outgrowth from GPR4-null aortas was less inhibited by acidic extracellular pH. Treatment with an analog of cAMP, a downstream effector of GPR4, abolished microvessel outgrowth bypassing the GPR4-knockout phenotype. These results suggest that GPR4 deficiency leads to partially penetrant vascular abnormalities during development and that this receptor functions in blood vessel pH sensing.
GPR4 is a G protein-coupled receptor expressed in the vasculature, lung, kidney, and other tissues. In vitro ectopic overexpression studies implicated GPR4 in sensing extracellular pH changes leading to cyclic AMP (cAMP) production. To investigate its biological roles in vivo, we generated GPR4-deficient mice by homologous recombination. Whereas GPR4-null adult mice appeared phenotypically normal, neonates showed a higher frequency of perinatal mortality. The average litter size from GPR4(-/-) intercrosses was approximately 30% smaller than that from GPR4(+/+) intercrosses on N3 and N5 C57BL/6 genetic backgrounds. A fraction of knockout embryos and neonates had spontaneous hemorrhages, dilated and tortuous subcutaneous blood vessels, and defective vascular smooth muscle cell coverage. Mesangial cells in kidney glomeruli were also significantly reduced in GPR4-null neonates. Some neonates exhibited respiratory distress with airway lining cell metaplasia. To examine whether GPR4 is functionally involved in vascular pH sensing, an ex vivo aortic ring assay was used under defined pH conditions. Compared to wild-type aortas, microvessel outgrowth from GPR4-null aortas was less inhibited by acidic extracellular pH. Treatment with an analog of cAMP, a downstream effector of GPR4, abolished microvessel outgrowth bypassing the GPR4-knockout phenotype. These results suggest that GPR4 deficiency leads to partially penetrant vascular abnormalities during development and that this receptor functions in blood vessel pH sensing.
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue MCB About MCB Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy MCB RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0270-7306 Online ISSN: 1098-5549 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to MCB .asm.org, visit: MCB       
GPR4 is a G protein-coupled receptor expressed in the vasculature, lung, kidney, and other tissues. In vitro ectopic overexpression studies implicated GPR4 in sensing extracellular pH changes leading to cyclic AMP (cAMP) production. To investigate its biological roles in vivo, we generated GPR4-deficient mice by homologous recombination. Whereas GPR4-null adult mice appeared phenotypically normal, neonates showed a higher frequency of perinatal mortality. The average litter size from GPR4 super(-/-) intercrosses was similar to 30% smaller than that from GPR4 super(+/+) intercrosses on N3 and N5 C57BL/6 genetic backgrounds. A fraction of knockout embryos and neonates had spontaneous hemorrhages, dilated and tortuous subcutaneous blood vessels, and defective vascular smooth muscle cell coverage. Mesangial cells in kidney glomeruli were also significantly reduced in GPR4-null neonates. Some neonates exhibited respiratory distress with airway lining cell metaplasia. To examine whether GPR4 is functionally involved in vascular pH sensing, an ex vivo aortic ring assay was used under defined pH conditions. Compared to wild-type aortas, microvessel outgrowth from GPR4-null aortas was less inhibited by acidic extracellular pH. Treatment with an analog of cAMP, a downstream effector of GPR4, abolished microvessel outgrowth bypassing the GPR4-knockout phenotype. These results suggest that GPR4 deficiency leads to partially penetrant vascular abnormalities during development and that this receptor functions in blood vessel pH sensing.
Author Meenakshi Roy
Owen N. Witte
Michael A. Teitell
Sunyoung Lee
Jami McLaughlin
M. Luisa Iruela-Arispe
Caius G. Radu
Li V. Yang
AuthorAffiliation Howard Hughes Medical Institute, 1 Department of Molecular and Medical Pharmacology, 2 Department of Chemistry and Biochemistry, 3 Department of Molecular, Cell and Developmental Biology, 4 Department of Microbiology, Immunology and Molecular Genetics, 5 Department of Pathology and Laboratory Medicine, University of California—Los Angeles, Los Angeles, California 90095 6
AuthorAffiliation_xml – name: Howard Hughes Medical Institute, 1 Department of Molecular and Medical Pharmacology, 2 Department of Chemistry and Biochemistry, 3 Department of Molecular, Cell and Developmental Biology, 4 Department of Microbiology, Immunology and Molecular Genetics, 5 Department of Pathology and Laboratory Medicine, University of California—Los Angeles, Los Angeles, California 90095 6
Author_xml – sequence: 1
  givenname: Li V.
  surname: Yang
  fullname: Yang, Li V.
  organization: Howard Hughes Medical Institute
– sequence: 2
  givenname: Caius G.
  surname: Radu
  fullname: Radu, Caius G.
  organization: Department of Molecular and Medical Pharmacology
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  givenname: Meenakshi
  surname: Roy
  fullname: Roy, Meenakshi
  organization: Department of Chemistry and Biochemistry
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  givenname: Sunyoung
  surname: Lee
  fullname: Lee, Sunyoung
  organization: Department of Molecular, Cell and Developmental Biology
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  givenname: Jami
  surname: McLaughlin
  fullname: McLaughlin, Jami
  organization: Department of Microbiology, Immunology and Molecular Genetics
– sequence: 6
  givenname: Michael A.
  surname: Teitell
  fullname: Teitell, Michael A.
  organization: Department of Pathology and Laboratory Medicine, University of California-Los Angeles
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  givenname: M. Luisa
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  givenname: Owen N.
  surname: Witte
  fullname: Witte, Owen N.
  email: owenw@microbio.ucla.edu
  organization: Department of Microbiology, Immunology and Molecular Genetics
BackLink https://www.ncbi.nlm.nih.gov/pubmed/17145776$$D View this record in MEDLINE/PubMed
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Corresponding author. Mailing address: Howard Hughes Medical Institute, University of California, Los Angeles, 675 Charles E. Young Drive South, 5-748 MRL Bldg., Los Angeles, CA 90095-1662. Phone: (310) 206-0386. Fax: (310) 206-8822. E-mail: owenw@microbio.ucla.edu.
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SSID ssj0006903
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Snippet Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
GPR4 is a G protein-coupled receptor expressed in the vasculature, lung, kidney, and other tissues. In vitro ectopic overexpression studies implicated GPR4 in...
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crossref
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SourceType Open Access Repository
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StartPage 1334
SubjectTerms Animals
Animals, Newborn
Aorta - abnormalities
Blood Vessels - abnormalities
Blood Vessels - embryology
Cells, Cultured
Crosses, Genetic
Embryo, Mammalian - abnormalities
Embryo, Mammalian - blood supply
Embryo, Mammalian - pathology
Female
Gene Targeting
Genotype
Hemorrhage - congenital
Humans
Hydrogen-Ion Concentration
Litter Size
Lung - abnormalities
Lung - embryology
Lung - pathology
Male
Mesangial Cells - pathology
Mice
Mice, Inbred C57BL
Mice, Knockout
Penetrance
Receptors, G-Protein-Coupled - deficiency
Receptors, G-Protein-Coupled - metabolism
Respiratory Tract Diseases - congenital
Title Vascular Abnormalities in Mice Deficient for the G Protein-Coupled Receptor GPR4 That Functions as a pH Sensor
URI http://mcb.asm.org/content/27/4/1334.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.01909-06
https://www.ncbi.nlm.nih.gov/pubmed/17145776
https://search.proquest.com/docview/19540178
https://search.proquest.com/docview/68959839
https://pubmed.ncbi.nlm.nih.gov/PMC1800706
Volume 27
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