The classical pink-eyed dilution mutation affects angiogenic responsiveness

Angiogenesis is the process by which new blood vessels are formed from existing vessels. Mammalian populations, including humans and mice, harbor genetic variations that alter angiogenesis. Angiogenesis-regulating gene variants can result in increased susceptibility to multiple angiogenesis-dependen...

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Published inPloS one Vol. 7; no. 5; p. e35237
Main Authors Rogers, Michael S, Boyartchuk, Victor, Rohan, Richard M, Birsner, Amy E, Dietrich, William F, D'Amato, Robert J
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 15.05.2012
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Abstract Angiogenesis is the process by which new blood vessels are formed from existing vessels. Mammalian populations, including humans and mice, harbor genetic variations that alter angiogenesis. Angiogenesis-regulating gene variants can result in increased susceptibility to multiple angiogenesis-dependent diseases in humans. Our efforts to dissect the complexity of the genetic diversity that regulates angiogenesis have used laboratory animals due to the availability of genome sequence for many species and the ability to perform high volume controlled breeding. Using the murine corneal micropocket assay, we have observed more than ten-fold difference in angiogenic responsiveness among various mouse strains. This degree of difference is observed with either bFGF or VEGF induced corneal neovascularization. Ongoing mapping studies have identified multiple loci that affect angiogenic responsiveness in several mouse models. In this study, we used F2 intercrosses between C57BL/6J and the 129 substrains 129P1/ReJ and 129P3/J, as well as the SJL/J strain, where we have identified new QTLs that affect angiogenic responsiveness. In the case of AngFq5, on chromosome 7, congenic animals were used to confirm the existence of this locus and subcongenic animals, combined with a haplotype-based mapping approach that identified the pink-eyed dilution mutation as a candidate polymorphism to explain AngFq5. The ability of mutations in the pink-eyed dilution gene to affect angiogenic response was demonstrated using the p-J allele at the same locus. Using this allele, we demonstrate that pink-eyed dilution mutations in Oca2 can affect both bFGF and VEGF-induced corneal angiogenesis.
AbstractList Angiogenesis is the process by which new blood vessels are formed from existing vessels. Mammalian populations, including humans and mice, harbor genetic variations that alter angiogenesis. Angiogenesis-regulating gene variants can result in increased susceptibility to multiple angiogenesis-dependent diseases in humans. Our efforts to dissect the complexity of the genetic diversity that regulates angiogenesis have used laboratory animals due to the availability of genome sequence for many species and the ability to perform high volume controlled breeding. Using the murine corneal micropocket assay, we have observed more than ten-fold difference in angiogenic responsiveness among various mouse strains. This degree of difference is observed with either bFGF or VEGF induced corneal neovascularization. Ongoing mapping studies have identified multiple loci that affect angiogenic responsiveness in several mouse models. In this study, we used F2 intercrosses between C57BL/6J and the 129 substrains 129P1/ReJ and 129P3/J, as well as the SJL/J strain, where we have identified new QTLs that affect angiogenic responsiveness. In the case of AngFq5, on chromosome 7, congenic animals were used to confirm the existence of this locus and subcongenic animals, combined with a haplotype-based mapping approach that identified the pink-eyed dilution mutation as a candidate polymorphism to explain AngFq5. The ability of mutations in the pink-eyed dilution gene to affect angiogenic response was demonstrated using the p-J allele at the same locus. Using this allele, we demonstrate that pink-eyed dilution mutations in Oca2 can affect both bFGF and VEGF-induced corneal angiogenesis.
Angiogenesis is the process by which new blood vessels are formed from existing vessels. Mammalian populations, including humans and mice, harbor genetic variations that alter angiogenesis. Angiogenesis-regulating gene variants can result in increased susceptibility to multiple angiogenesis-dependent diseases in humans. Our efforts to dissect the complexity of the genetic diversity that regulates angiogenesis have used laboratory animals due to the availability of genome sequence for many species and the ability to perform high volume controlled breeding. Using the murine corneal micropocket assay, we have observed more than ten-fold difference in angiogenic responsiveness among various mouse strains. This degree of difference is observed with either bFGF or VEGF induced corneal neovascularization. Ongoing mapping studies have identified multiple loci that affect angiogenic responsiveness in several mouse models. In this study, we used F2 intercrosses between C57BL/6J and the 129 substrains 129P1/ReJ and 129P3/J, as well as the SJL/J strain, where we have identified new QTLs that affect angiogenic responsiveness. In the case of AngFq5 , on chromosome 7, congenic animals were used to confirm the existence of this locus and subcongenic animals, combined with a haplotype-based mapping approach that identified the pink-eyed dilution mutation as a candidate polymorphism to explain AngFq5. The ability of mutations in the pink-eyed dilution gene to affect angiogenic response was demonstrated using the p-J allele at the same locus. Using this allele, we demonstrate that pink-eyed dilution mutations in Oca2 can affect both bFGF and VEGF-induced corneal angiogenesis.
Audience Academic
Author Rogers, Michael S
Dietrich, William F
Boyartchuk, Victor
Rohan, Richard M
D'Amato, Robert J
Birsner, Amy E
AuthorAffiliation Purdue University, United States of America
3 Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America
1 Vascular Biology Program, Children’s Hospital Boston, Boston, Massachusetts, United States of America
2 Department of Surgery, Harvard Medical School, Boston, Massachusetts, United States of America
4 Program in Gene Function and Expression, UMass Medical School, Worcester, Massachusetts, United States of America
5 Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, United States of America
AuthorAffiliation_xml – name: Purdue University, United States of America
– name: 4 Program in Gene Function and Expression, UMass Medical School, Worcester, Massachusetts, United States of America
– name: 5 Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, United States of America
– name: 1 Vascular Biology Program, Children’s Hospital Boston, Boston, Massachusetts, United States of America
– name: 3 Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, United States of America
– name: 2 Department of Surgery, Harvard Medical School, Boston, Massachusetts, United States of America
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  givenname: Michael S
  surname: Rogers
  fullname: Rogers, Michael S
  email: michael.rogers@childrens.harvard.edu
  organization: Vascular Biology Program, Children's Hospital Boston, Boston, Massachusetts, United States of America. michael.rogers@childrens.harvard.edu
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  givenname: Victor
  surname: Boyartchuk
  fullname: Boyartchuk, Victor
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  givenname: Richard M
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  givenname: Amy E
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Copyright COPYRIGHT 2012 Public Library of Science
2012 Rogers et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Rogers et al. 2012
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– notice: 2012 Rogers et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Snippet Angiogenesis is the process by which new blood vessels are formed from existing vessels. Mammalian populations, including humans and mice, harbor genetic...
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StartPage e35237
SubjectTerms Alleles
Angiogenesis
Animal models
Animals
Biology
Blood vessels
Breeding
Cancer
Chromosome 7
Cornea
Dilution
Disease susceptibility
Dopamine
Eye Color - genetics
Fibroblast growth factor 2
Fibroblast growth factors
Gene mapping
Genes
Genetic aspects
Genetic diversity
Genetic polymorphisms
Genomes
Genomics
Haplotypes
Heart
House mouse
Hypoxia
Ischemia
Laboratory animals
Laboratory tests
Mapping
Medical schools
Medicine
Melanoma
Mice
Mice, Inbred C57BL
Mutation
Neovascularization
Neovascularization, Physiologic - genetics
Nucleotide sequence
Permeability
Polymorphism
Polymorphism, Genetic
Proteins
Quantitative trait loci
Rodents
Smooth muscle
Stability
Vascular endothelial growth factor
Vascularization
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Title The classical pink-eyed dilution mutation affects angiogenic responsiveness
URI https://www.ncbi.nlm.nih.gov/pubmed/22615734
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https://doaj.org/article/3788edd0b3a041e68f35fae8e3eba6ff
http://dx.doi.org/10.1371/journal.pone.0035237
Volume 7
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