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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

Vascular remodeling defects seen in ErgΔEx4/ΔEx4 embryos at E10.5. (A,B) CD31 staining shows that mutant yolk sac (B) lacks larger vessels, displaying only a capillary plexus when compared with controls that display a well-organized vasculature (A). (C,D) ErgΔEx4/ΔEx4 embryos show vascular remodeling abnormalities in the head (D), failing to exhibit normal alignment and invasion of vessels from the perineural vascular plexus into the developing ganglionic eminence, as seen in controls (C) (arrowheads). Insets are low-magnification images of the head. (E,F) CD31 staining of vasculature in the placental labyrinth at E10.5 shows abundant vessels in ErgΔEx4/+ (E), whereas the ErgΔEx4/ΔEx4 embryos display collapsed and pooled vessels (F).
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Figure 6: Vascular remodeling defects seen in ErgΔEx4/ΔEx4 embryos at E10.5. (A,B) CD31 staining shows that mutant yolk sac (B) lacks larger vessels, displaying only a capillary plexus when compared with controls that display a well-organized vasculature (A). (C,D) ErgΔEx4/ΔEx4 embryos show vascular remodeling abnormalities in the head (D), failing to exhibit normal alignment and invasion of vessels from the perineural vascular plexus into the developing ganglionic eminence, as seen in controls (C) (arrowheads). Insets are low-magnification images of the head. (E,F) CD31 staining of vasculature in the placental labyrinth at E10.5 shows abundant vessels in ErgΔEx4/+ (E), whereas the ErgΔEx4/ΔEx4 embryos display collapsed and pooled vessels (F).

Mentions: Vascular defects in the ErgΔEx4/ΔEx4 embryos were observed as early as E10.5. The large arborized vessels that are characteristic of the remodeled vascular plexus were completely absent in the yolk sac of ErgΔEx4/ΔEx4 embryos (Fig. 6B). Whole-mount CD31 (Pecam1) staining of the ErgΔEx4/ΔEx4 yolk sac revealed that the primary capillary plexuses were present but that these capillaries failed to fuse into the larger vessels seen in the controls (Fig. 6B), indicating a vascular remodeling defect.


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)

Vascular remodeling defects seen in ErgΔEx4/ΔEx4 embryos at E10.5. (A,B) CD31 staining shows that mutant yolk sac (B) lacks larger vessels, displaying only a capillary plexus when compared with controls that display a well-organized vasculature (A). (C,D) ErgΔEx4/ΔEx4 embryos show vascular remodeling abnormalities in the head (D), failing to exhibit normal alignment and invasion of vessels from the perineural vascular plexus into the developing ganglionic eminence, as seen in controls (C) (arrowheads). Insets are low-magnification images of the head. (E,F) CD31 staining of vasculature in the placental labyrinth at E10.5 shows abundant vessels in ErgΔEx4/+ (E), whereas the ErgΔEx4/ΔEx4 embryos display collapsed and pooled vessels (F).
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 6: Vascular remodeling defects seen in ErgΔEx4/ΔEx4 embryos at E10.5. (A,B) CD31 staining shows that mutant yolk sac (B) lacks larger vessels, displaying only a capillary plexus when compared with controls that display a well-organized vasculature (A). (C,D) ErgΔEx4/ΔEx4 embryos show vascular remodeling abnormalities in the head (D), failing to exhibit normal alignment and invasion of vessels from the perineural vascular plexus into the developing ganglionic eminence, as seen in controls (C) (arrowheads). Insets are low-magnification images of the head. (E,F) CD31 staining of vasculature in the placental labyrinth at E10.5 shows abundant vessels in ErgΔEx4/+ (E), whereas the ErgΔEx4/ΔEx4 embryos display collapsed and pooled vessels (F).
Mentions: Vascular defects in the ErgΔEx4/ΔEx4 embryos were observed as early as E10.5. The large arborized vessels that are characteristic of the remodeled vascular plexus were completely absent in the yolk sac of ErgΔEx4/ΔEx4 embryos (Fig. 6B). Whole-mount CD31 (Pecam1) staining of the ErgΔEx4/ΔEx4 yolk sac revealed that the primary capillary plexuses were present but that these capillaries failed to fuse into the larger vessels seen in the controls (Fig. 6B), indicating a vascular remodeling defect.

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