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Erg is a crucial regulator of endocardial-mesenchymal transformation during cardiac valve morphogenesis.

Vijayaraj P, Le Bras A, Mitchell N, Kondo M, Juliao S, Wasserman M, Beeler D, Spokes K, Aird WC, Baldwin HS, Oettgen P - Development (2012)

Bottom Line: Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes.The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells.We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

ABSTRACT
During murine embryogenesis, the Ets factor Erg is highly expressed in endothelial cells of the developing vasculature and in articular chondrocytes of developing bone. We identified seven isoforms for the mouse Erg gene. Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes. The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells. Homozygous Erg(ΔEx3/ΔEx3) knockout mice are viable, fertile and do not display any overt phenotype. By contrast, homozygous Erg(ΔEx4/ΔEx4) knockout mice are embryonic lethal, which is associated with a marked reduction in endocardial-mesenchymal transformation (EnMT) during cardiac valve morphogenesis. We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

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Related in: MedlinePlus

Placental vascular defects in ErgΔEx4/ΔEx4 embryos at E10. (A,B) The dashed lines in Erg+/+ (A) and ErgΔEx4/ΔEx4 (B) indicate the extent of decidual invasion in each placental section. (C,D) Magnification of the boxed areas in A and B. Well-defined vasculature is observed in Erg+/+ placentas (C), whereas the mutants, although they have abundant maternal blood sinuses, lack well-defined fetal-derived capillaries (D). (E,F) Higher magnification of C and D reveal abundant nucleated fetal blood in the controls (arrows, E), whereas the mutants show a drastic reduction in the number of fetal blood cells and exhibit collapsed capillaries (arrows, F). D, maternal decidua; L, labyrinth; E, embryo; MB, maternal blood; EB, embryonic blood.
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Figure 8: Placental vascular defects in ErgΔEx4/ΔEx4 embryos at E10. (A,B) The dashed lines in Erg+/+ (A) and ErgΔEx4/ΔEx4 (B) indicate the extent of decidual invasion in each placental section. (C,D) Magnification of the boxed areas in A and B. Well-defined vasculature is observed in Erg+/+ placentas (C), whereas the mutants, although they have abundant maternal blood sinuses, lack well-defined fetal-derived capillaries (D). (E,F) Higher magnification of C and D reveal abundant nucleated fetal blood in the controls (arrows, E), whereas the mutants show a drastic reduction in the number of fetal blood cells and exhibit collapsed capillaries (arrows, F). D, maternal decidua; L, labyrinth; E, embryo; MB, maternal blood; EB, embryonic blood.

Mentions: We also observed defective vasculature in the labyrinth region of the placenta in ErgΔEx4/ΔEx4 embryos. Whereas the controls displayed normal placental villi and capillaries, in the ErgΔEx4/ΔEx4 placentas the capillaries were not clearly discernible by CD31 staining (Fig. 7F). Instead, the placental capillaries appeared collapsed, with a drastic reduction in fetal blood (Fig. 8F, arrows), possibly a consequence of abnormal cardiac function and circulatory collapse. Taken together, these results indicate that the vasculature in both the embryo and extra-embryonic tissues of ErgΔEx4/ΔEx4 has vascular remodeling defects.


Erg is a crucial regulator of endocardial-mesenchymal transformation during cardiac valve morphogenesis.

Vijayaraj P, Le Bras A, Mitchell N, Kondo M, Juliao S, Wasserman M, Beeler D, Spokes K, Aird WC, Baldwin HS, Oettgen P - Development (2012)

Placental vascular defects in ErgΔEx4/ΔEx4 embryos at E10. (A,B) The dashed lines in Erg+/+ (A) and ErgΔEx4/ΔEx4 (B) indicate the extent of decidual invasion in each placental section. (C,D) Magnification of the boxed areas in A and B. Well-defined vasculature is observed in Erg+/+ placentas (C), whereas the mutants, although they have abundant maternal blood sinuses, lack well-defined fetal-derived capillaries (D). (E,F) Higher magnification of C and D reveal abundant nucleated fetal blood in the controls (arrows, E), whereas the mutants show a drastic reduction in the number of fetal blood cells and exhibit collapsed capillaries (arrows, F). D, maternal decidua; L, labyrinth; E, embryo; MB, maternal blood; EB, embryonic blood.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3472597&req=5

Figure 8: Placental vascular defects in ErgΔEx4/ΔEx4 embryos at E10. (A,B) The dashed lines in Erg+/+ (A) and ErgΔEx4/ΔEx4 (B) indicate the extent of decidual invasion in each placental section. (C,D) Magnification of the boxed areas in A and B. Well-defined vasculature is observed in Erg+/+ placentas (C), whereas the mutants, although they have abundant maternal blood sinuses, lack well-defined fetal-derived capillaries (D). (E,F) Higher magnification of C and D reveal abundant nucleated fetal blood in the controls (arrows, E), whereas the mutants show a drastic reduction in the number of fetal blood cells and exhibit collapsed capillaries (arrows, F). D, maternal decidua; L, labyrinth; E, embryo; MB, maternal blood; EB, embryonic blood.
Mentions: We also observed defective vasculature in the labyrinth region of the placenta in ErgΔEx4/ΔEx4 embryos. Whereas the controls displayed normal placental villi and capillaries, in the ErgΔEx4/ΔEx4 placentas the capillaries were not clearly discernible by CD31 staining (Fig. 7F). Instead, the placental capillaries appeared collapsed, with a drastic reduction in fetal blood (Fig. 8F, arrows), possibly a consequence of abnormal cardiac function and circulatory collapse. Taken together, these results indicate that the vasculature in both the embryo and extra-embryonic tissues of ErgΔEx4/ΔEx4 has vascular remodeling defects.

Bottom Line: Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes.The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells.We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

ABSTRACT
During murine embryogenesis, the Ets factor Erg is highly expressed in endothelial cells of the developing vasculature and in articular chondrocytes of developing bone. We identified seven isoforms for the mouse Erg gene. Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes. The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells. Homozygous Erg(ΔEx3/ΔEx3) knockout mice are viable, fertile and do not display any overt phenotype. By contrast, homozygous Erg(ΔEx4/ΔEx4) knockout mice are embryonic lethal, which is associated with a marked reduction in endocardial-mesenchymal transformation (EnMT) during cardiac valve morphogenesis. We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

Show MeSH
Related in: MedlinePlus