scholarly journals Vascular dimorphism ensured by regulated proteoglycan dynamics favors rapid umbilical artery closure at birth

2020 ◽  
Author(s):  
Sumeda Nandadasa ◽  
Jason M. Szafron ◽  
Vai Pathak ◽  
Sae-Il Murtada ◽  
Caroline M. Kraft ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Blood Loss ◽  
Computational Analysis ◽  
Umbilical Artery ◽  
Umbilical Vein ◽  
Mammalian Evolution ◽  
Vascular Responses ◽  
Umbilical Vessel ◽  
Arterial Lumen ◽  
Selection Step

AbstractThe umbilical artery lumen occludes rapidly at birth, preventing blood loss, whereas the umbilical vein remains patent, providing the newborn with a placental infusion. Here, we identify differential arterial-venous proteoglycan dynamics as a determinant of these contrasting vascular responses. We show that the umbilical artery, unlike the vein, has an inner layer enriched in the hydrated proteoglycan aggrecan, external to which lie contraction-primed smooth muscle cells (SMC). At birth, SMC contraction drives inner layer buckling and centripetal displacement to occlude the arterial lumen, a mechanism elicited by biomechanical and computational analysis. Vascular dimorphism arises from spatially regulated proteoglycan expression and breakdown in umbilical vessels. Mice lacking aggrecan or the metalloprotease ADAMTS1, which degrades proteoglycans, demonstrated their opposing roles in umbilical cord arterial-venous dimorphism and contrasting effects on SMC differentiation. Umbilical vessel dimorphism is conserved in mammals, suggesting that their differential proteoglycan dynamics were a positive selection step in mammalian evolution.

scholarly journals Vascular dimorphism ensured by regulated proteoglycan dynamics favors rapid umbilical artery closure at birth

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Sumeda Nandadasa ◽  
Jason M Szafron ◽  
Vai Pathak ◽  
Sae-Il Murtada ◽  
Caroline M Kraft ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Blood Loss ◽  
Umbilical Artery ◽  
Umbilical Vein ◽  
Vascular Responses ◽  
Umbilical Vessel ◽  
Arterial Lumen ◽  
Neonatal Blood ◽  
Computational Analyses ◽  
Umbilical Cords

The umbilical artery lumen closes rapidly at birth, preventing neonatal blood loss, whereas the umbilical vein remains patent longer. Here, analysis of umbilical cords from humans and other mammals identified differential arterial-venous proteoglycan dynamics as a determinant of these contrasting vascular responses. The umbilical artery, but not the vein, has an inner layer enriched in the hydrated proteoglycan aggrecan, external to which lie contraction-primed smooth muscle cells (SMC). At birth, SMC contraction drives inner layer buckling and centripetal displacement to occlude the arterial lumen, a mechanism revealed by biomechanical observations and confirmed by computational analyses. This vascular dimorphism arises from spatially regulated proteoglycan expression and breakdown. Mice lacking aggrecan or the metalloprotease ADAMTS1, which degrades proteoglycans, demonstrate their opposing roles in umbilical vascular dimorphism, including effects on SMC differentiation. Umbilical vessel dimorphism is conserved in mammals, suggesting that differential proteoglycan dynamics and inner layer buckling were positively selected during evolution.

UMBILICAL VESSEL ANGIOCARDIOGRAPHY IN THE NEWBORN INFANT

PEDIATRICS ◽  
1963 ◽  
Vol 31 (6) ◽  
pp. 946-951
Author(s):  
Samuel O. Sapin ◽  
Leonard M. Linde ◽  
George C. Emmanouilides
Keyword(s):  
Newborn Infant ◽  
Umbilical Artery ◽  
Umbilical Vein ◽  
Newborn Infants ◽  
Umbilical Vessel ◽  
Accurate Interpretation ◽  
Sick Newborn

Angiocardiography from an umbilical vessel approach was performed in 10 critically sick newborn infants. The umbilical vein route was successfully employed up to the eighth day of life, while the umbilical artery was safely used as late as age 5 days. This approach has advantages over other methods of catheterization and angiocardiography. Angiocardiographic quality was satisfactory for accurate interpretation.

Postnatal dilatation of umbilical cord vessels and its impact on wall integrity: Prerequisite for the artificial placenta

2018 ◽  
Vol 41 (7) ◽  
pp. 393-399 ◽  
Author(s):  
Jenny Peng ◽  
Niels Rochow ◽  
Mohammadhossein Dabaghi ◽  
Radenka Bozanovic ◽  
Jan Jansen ◽  
...  
Keyword(s):  
Umbilical Artery ◽  
Umbilical Vein ◽  
Transluminal Angioplasty ◽  
Assist Device ◽  
Umbilical Vessels ◽  
Umbilical Vessel ◽  
Vessel Integrity ◽  
And Control ◽  
The Impact ◽  
Control Samples

Introduction: A lung assist device, which acts as an artificial placenta, can provide additional gas exchange for preterm and term newborns with respiratory failure. The concept of the lung assist device requires a large bore access via umbilical vessels to allow pumpless extracorporeal blood flow rates up to 30 mL/kg/min. After birth, constricted umbilical vessels need to be reopened for vascular access. The objective is to study the impact of umbilical vessel expansion on vessel integrity for achieving large bore access. Methods: Umbilical cords from healthy term deliveries were cannulated and dilatated with percutaneous transluminal angioplasty catheters in 1 mm increments from 4 to 8 mm for umbilical artery and from 4 to 15 mm for umbilical vein, n = 6 per expansion diameter. Paraffin-embedded transverse sections of dilated and control samples were HE & Van Gieson stained. Effects of dilatation, shown by splitting, were measured. Results: Umbilical vessel expansion led to concentric splitting, shown by areas devoid of extracellular matrix and nuclei in the tunica intima and media. No radial splitting was observed. Results suggest an expansion threshold of umbilical artery at 6 mm and umbilical vein at 7 mm, while maximal splitting was observed above this threshold (3.6 ± 0.8%, p = 0.043 for umbilical artery 7 mm and 6.3 ± 1.8%, p = 0.048 for umbilical vein 8 mm). Endothelial cell sloughing was present in all dilated samples but not in the control samples. Conclusion: The suggested thresholds for safe expansions are similar to in utero umbilical vessel diameters and demonstrate a proof of concept for attaining large bore access for the lung assist device.

Contamination of Umbilical Vessel Catheters: Encouraging Information

PEDIATRICS ◽  
1972 ◽  
Vol 49 (3) ◽  
pp. 470-471
Author(s):  
William F. Powers ◽  
William H. Tooley
Keyword(s):  
Bacterial Contamination ◽  
Umbilical Artery ◽  
Umbilical Vein ◽  
Bacterial Colonization ◽  
Significant Risk ◽  
The Other ◽  
Umbilical Vessel ◽  
Other Hand ◽  
Umbilical Artery Catheterization ◽  
Recent Editorial

In his recent editorial, Dr. Cook1 mentions bacterial contamination as one of the complications of umbilical artery catheterization, and refers to a report by Krauss, et al.2 who grew bacteria from 6 of 11 (55%) umbilical artery catheters. Balagtas, et al.3 have also published similar findings with umbilical vein catheters, 52% of which had bacterial colonization on removal. These reports stress the significant risk of generalized infection with umbilical vessel catheters. On the other hand, Casalino and Lipsitz4 report a 5% incidence of bacterial contamination.

scholarly journals Expression of the CD34 gene in vascular endothelial cells

Blood ◽  
1990 ◽  
Vol 75 (12) ◽  
pp. 2417-2426 ◽  
Author(s):  
L Fina ◽  
HV Molgaard ◽  
D Robertson ◽  
NJ Bradley ◽  
P Monaghan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelium ◽  
Umbilical Artery ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Endothelial ◽  
Umbilical Vessel ◽  
Cd34 Antigen ◽  
Large Vessels ◽  
Hemopoietic Progenitor

Abstract All seven of a set of CD34 monoclonal antibodies that recognize epitopes on an approximately 110 Kd glycoprotein on human hemopoietic progenitor cells also bind to vascular endothelium. Capillaries of most tissues are CD34 positive, as are umbilical artery and, to a lesser extent, vein, but the endothelium of most large vessels and the endothelium of placental sinuses are not. Angioblastoma cells and parafollicular mesenchymal cells in fetal skin are also CD34 positive, as are some stromal elements. An approximately 110 Kd protein can be identified by Western blot analysis with CD34 antibodies in detergent extracts of freshly isolated umbilical vessel endothelial cells, and CD34 mRNA is present in cultured umbilical vein cells as well as other tissues rich in vascular endothelium (breast, placenta). These data indicate that the binding of CD34 antibodies to vascular endothelium is to the CD34 gene product, and not to crossreactive epitopes. Despite the presence of CD34 mRNA in cultured, proliferating endothelial cells, the latter do not bind CD34 antibodies. In addition, CD34 antigen cannot be upregulated by growth factors. We conclude that under these conditions, CD34 protein is downregulated or processed into another form that is unreactive with CD34 antibodies. Electron microscopy of umbilical artery, breast, and kidney capillary vessels reveals that in all three sites, CD34 molecules are concentrated on membrane processes, many of which interdigitate between adjacent endothelial cells. However, well-established endothelial cell contacts with tight junctions are CD34 negative. CD34 may function as an adhesion molecule on both endothelial cells and hematopoietic progenitors.

scholarly journals Expression of the CD34 gene in vascular endothelial cells

Blood ◽  
1990 ◽  
Vol 75 (12) ◽  
pp. 2417-2426 ◽  
Author(s):  
L Fina ◽  
HV Molgaard ◽  
D Robertson ◽  
NJ Bradley ◽  
P Monaghan ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelium ◽  
Umbilical Artery ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Vascular Endothelial ◽  
Umbilical Vessel ◽  
Cd34 Antigen ◽  
Large Vessels ◽  
Hemopoietic Progenitor

All seven of a set of CD34 monoclonal antibodies that recognize epitopes on an approximately 110 Kd glycoprotein on human hemopoietic progenitor cells also bind to vascular endothelium. Capillaries of most tissues are CD34 positive, as are umbilical artery and, to a lesser extent, vein, but the endothelium of most large vessels and the endothelium of placental sinuses are not. Angioblastoma cells and parafollicular mesenchymal cells in fetal skin are also CD34 positive, as are some stromal elements. An approximately 110 Kd protein can be identified by Western blot analysis with CD34 antibodies in detergent extracts of freshly isolated umbilical vessel endothelial cells, and CD34 mRNA is present in cultured umbilical vein cells as well as other tissues rich in vascular endothelium (breast, placenta). These data indicate that the binding of CD34 antibodies to vascular endothelium is to the CD34 gene product, and not to crossreactive epitopes. Despite the presence of CD34 mRNA in cultured, proliferating endothelial cells, the latter do not bind CD34 antibodies. In addition, CD34 antigen cannot be upregulated by growth factors. We conclude that under these conditions, CD34 protein is downregulated or processed into another form that is unreactive with CD34 antibodies. Electron microscopy of umbilical artery, breast, and kidney capillary vessels reveals that in all three sites, CD34 molecules are concentrated on membrane processes, many of which interdigitate between adjacent endothelial cells. However, well-established endothelial cell contacts with tight junctions are CD34 negative. CD34 may function as an adhesion molecule on both endothelial cells and hematopoietic progenitors.

Complications of Umbilical Vessel Catheterization: Peritoneal Perforation

PEDIATRICS ◽  
1969 ◽  
Vol 44 (6) ◽  
pp. 1028-1030
Author(s):  
G. Van Leeuwen ◽  
M. Patney
Keyword(s):  
Umbilical Artery ◽  
Community Hospital ◽  
Umbilical Vein ◽  
Potential Danger ◽  
Umbilical Vessel ◽  
Reticular Pattern ◽  
Vein Catheter ◽  
Peritoneal Perforation ◽  
Umbilical Artery Catheterization ◽  
Umbilical Vein Catheter

Umbilical artery catheterization has been performed for approximately 6 years for diagnostic and investigative studies, and more recently for intravascular fluid therapy. We recently encountered a complication—perforation of the peritoneum—which illustrates another potential danger of this procedure. CASE REPORT Baby Y., a 1,590 gm female infant, was delivered in a community hospital. She was delivered with membranes intact but aspirated amniotic fluid containing meconium when the membranes were removed. At 20 minutes of age examination revealed marked intercostal retractions, a respiratory rate of 60 per minute, and cyanosis. Roentgenograms of the chest showed a fine reticular pattern. An umbilical vein catheter was inserted, but blood could not be aspirated.

scholarly journals LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs

Open Medicine ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. 117-127
Author(s):  
Hongmei Gao ◽  
Zhaohui Guo
Keyword(s):  
Smooth Muscle ◽  
Muscle Protein ◽  
Umbilical Vein ◽  
Smooth Muscle Actin ◽  
Quantitative Polymerase Chain Reaction ◽  
Density Lipoprotein ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Western Blot Assay ◽  
Lactate Dehydrogenase Activity

Abstract Long noncoding RNAs (lncRNAs) have been verified as vital regulators in human disease, including atherosclerosis. However, the precise role of X-inactive-specific transcript (XIST) in atherosclerosis remains unclear. The proliferation and apoptosis of human umbilical vein endothelial cells (HUVECs) exposed to low-density lipoprotein (ox-LDL) were assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide, and flow cytometry assays, correspondingly. The western blot assay was used to quantify protein expression. Lactate dehydrogenase activity and the concentrations of inflammatory factors were measured by matched kits. The real-time quantitative polymerase chain reaction (qPCR) was used to determine α-smooth muscle actin, smooth muscle protein 22-α, XIST, miR-98-5p, and pregnancy-associated plasma protein A (PAPPA) levels in HUVECs. The relationship among XIST, miR-98-5p, and PAPPA was analyzed by dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. We found ox-LDL repressed proliferation and induced inflammation and apoptosis in HUVECs. Loss-of-functional experiment suggested that the downregulation of XIST overturned the ox-LDL-induced effects on HUVECs. Additionally, overexpression of miR-98-5p-induced effects on ox-LDL-stimulated HUVECs was abolished by upregulation of XIST. However, silencing of miR-98-5p strengthened the ox-LDL-induced effects on HUVECs by increasing expression of PAPPA. Mechanistically, XIST could regulate PAPPA expression in ox-LDL-induced HUVECs by sponging miR-98-5p, providing understanding for atherosclerosis.

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