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Comment
. 2020 Oct 12:9:e63128.
doi: 10.7554/eLife.63128.

Severing umbilical ties

Jessica E Wagenseil  1 , Karen M Downs  2
Affiliations
Comment

Severing umbilical ties

Jessica E Wagenseil et al. Elife. .

Abstract

High levels of proteins called proteoglycans in the walls of umbilical arteries enable these arteries to close rapidly after birth and thus prevent blood loss in newborns.

Keywords: birth; computational biology; developmental biology; extracellular matrix; human; mouse; proteoglycans; systems biology; umbilical cord; vascular engineering; vascular smooth muscle.

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Conflict of interest statement

JW, KD No competing interests declared

Figures

Figure 1.
Figure 1.. The morphology of the umbilical arteries before and after birth.
(A) Umbilical arteries (dark blue) transport oxygen and nutrient-depleted blood to the placenta, while the umbilical vein (dark red) carries oxygen and nutrients to the fetus. During pregnancy, the umbilical arteries (cross-section, left side) have a thickened middle layer (the tunica media), whose outer layer is populated with contractile smooth muscle cells (SMCs; orange) and whose inner layer contains a high levels of proteins known as proteoglycans (light blue). (B) At birth, the umbilical arteries close rapidly (indicated by the yellow x) to prevent blood loss in the newborn. This is caused by the high local concentrations of proteoglycans, which enable the inner layer of the tunica media to swell and help the smooth muscle cells to contract more strongly (cross section, right side).
See this image and copyright information in PMC

Comment on

References

    1. Hung Y-C, Yeh J-L, Hsu J-H. Molecular mechanisms for regulating postnatal ductus arteriosus closure. International Journal of Molecular Sciences. 2018;19:1861–1874. doi: 10.3390/ijms19071861. - DOI - PMC - PubMed
    1. Koch CD, Lee CM, Apte SS. Aggrecan in cardiovascular development and disease. Journal of Histochemistry & Cytochemistry. 2020;249:002215542095290. doi: 10.1369/0022155420952902. - DOI - PMC - PubMed
    1. Kwee L, Baldwin HS, Shen HM, Stewart CL, Buck C, Buck CA, Labow MA. Defective development of the embryonic and extraembryonic circulatory systems in vascular cell adhesion molecule (VCAM-1) deficient mice. Development. 1995;121:489–503. - PubMed
    1. Nandadasa S, Szafron JM, Pathak V, Murtada SI, Kraft CM, O'Donnell A, Norvik C, Hughes C, Caterson B, Domowicz MS, Schwartz NB, Tran-Lundmark K, Veigl M, Sedwick D, Philipson EH, Humphrey JD, Apte SS. Vascular dimorphism ensured by regulated proteoglycan dynamics favors rapid umbilical artery closure at birth. eLife. 2020;9:e60683. doi: 10.7554/eLife.60683. - DOI - PMC - PubMed
    1. Oller J, Méndez-Barbero N, Ruiz EJ, Villahoz S, Renard M, Canelas LI, Briones AM, Alberca R, Lozano-Vidal N, Hurlé MA, Milewicz D, Evangelista A, Salaices M, Nistal JF, Jiménez-Borreguero LJ, De Backer J, Campanero MR, Redondo JM. Nitric oxide mediates aortic disease in mice deficient in the metalloprotease Adamts1 and in a mouse model of marfan syndrome. Nature Medicine. 2017;23:200–212. doi: 10.1038/nm.4266. - DOI - PubMed