scholarly journals OC082: Vascular growth and function in late adolescence after intrauterine growth restriction

2004 ◽  
Vol 24 (3) ◽  
pp. 238-239
Author(s):  
J. Brodszki ◽  
D. Ley ◽  
T. Länne ◽  
K. Marsal
Circulation ◽  
2005 ◽  
Vol 111 (20) ◽  
pp. 2623-2628 ◽  
Author(s):  
J. Brodszki ◽  
T. Länne ◽  
K. Maršál ◽  
D. Ley

2018 ◽  
Vol 315 (3) ◽  
pp. L348-L359 ◽  
Author(s):  
R. Blair Dodson ◽  
Kyle N. Powers ◽  
Jason Gien ◽  
Paul J. Rozance ◽  
Gregory Seedorf ◽  
...  

Intrauterine growth restriction (IUGR) in premature newborns increases the risk for bronchopulmonary dysplasia, a chronic lung disease characterized by disrupted pulmonary angiogenesis and alveolarization. We previously showed that experimental IUGR impairs angiogenesis; however, mechanisms that impair pulmonary artery endothelial cell (PAEC) function are uncertain. The NF-κB pathway promotes vascular growth in the developing mouse lung, and we hypothesized that IUGR disrupts NF-κB-regulated proangiogenic targets in fetal PAEC. PAECs were isolated from the lungs of control fetal sheep and sheep with experimental IUGR from an established model of chronic placental insufficiency. Microarray analysis identified suppression of NF-κB signaling and significant alterations in extracellular matrix (ECM) pathways in IUGR PAEC, including decreases in collagen 4α1 and laminin α4, components of the basement membrane and putative NF-κB targets. In comparison with controls, immunostaining of active NF-κB complexes, NF-κB-DNA binding, baseline expression of NF-κB subunits p65 and p50, and LPS-mediated inducible activation of NF-κB signaling were decreased in IUGR PAEC. Although pharmacological NF-κB inhibition did not affect angiogenic function in IUGR PAEC, angiogenic function of control PAEC was reduced to a similar degree as that observed in IUGR PAEC. These data identify reductions in endothelial NF-κB signaling as central to the disrupted angiogenesis observed in IUGR, likely by impairing both intrinsic PAEC angiogenic function and NF-κB-mediated regulation of ECM components necessary for vascular development. These data further suggest that strategies that preserve endothelial NF-κB activation may be useful in lung diseases marked by disrupted angiogenesis such as IUGR.


2005 ◽  
Vol 73 (6) ◽  
pp. 1164-1173 ◽  
Author(s):  
Catrin S. Rutland ◽  
Mallinath Mukhopadhyay ◽  
Suzanne Underwood ◽  
Norma Clyde ◽  
Terry M. Mayhew ◽  
...  

2019 ◽  
Vol 21 (1) ◽  
pp. 62
Author(s):  
Gabriela Corina Zaharie ◽  
Monica Hasmasanu ◽  
Ligia Blaga ◽  
Melinda Matyas ◽  
Daniel Muresan ◽  
...  

Aim: To asses the cardiac morphology and functional changes specific for newborns from intrauterine growth restriction (IUGR) pregnancies.Material and method: A cohort of IUGR infants were evaluated by serial echocardiographies at delivery and at the first and six months follow-ups. IUGR newborn delivery status was compared to that of newborns in the control group according to gestational age (AGA).Results: Left heart measurements were significantly lower in IUGR newborns compared to AGA babies. Left ventricular size increased at follow-up inthe IUGR group (p<0.05). Systolic dysfunction (the myocardial performance index (MPI)> 0.47) was identified in 40% of the neonates in the IUGR group (16/40), respectively 4.76% in the control group. IUGR neonates had a significantly increased proportion of systolic malfunction (p=0.004).Conclusion: IUGR patients had reduced left ventricle dimensions compared to AGA babies. The MPI stands out as a marker of leftheart function in newborns. Systolic dysfunction was a hallmark of the cardiac adaptation in IUGR neonates. 


2014 ◽  
Vol 26 (1) ◽  
pp. 150
Author(s):  
P. Peugnet ◽  
S. Valentino ◽  
A. Tarrade ◽  
L. Wimel ◽  
F. Reigner ◽  
...  

In equids, placentation is diffuse and the nutrient supply to the fetus is determined by uterine size, which is correlated with maternal size. The size of the mare affects fetal development as shown by embryo transfer (ET) between Ponies and Thoroughbreds. In turn, insulin sensitivity in the newborn foal and subsequent postnatal growth rate are affected. We enhanced or restricted fetal growth through ET using Pony (P), Saddlebred (S), and Draft (D) horses and investigated placental morphology, structure, and function at term. Control pregnancies of P-P (n = 21), S-S (n = 28), and D-D (n = 8) were obtained by AI. Enhanced and restricted pregnancies were obtained by transferring P (P-D, n = 6) and S embryos (S-D, n = 8) into D mares or S embryos into P mares (S-P, n = 6), respectively. Placental weight and surface were recorded at delivery. Samples were collected for stereology and RT-qPCR analysis of expression of genes involved in placental growth, vascularization, and nutrient transport. Housekeeping genes were RPL32, SCAMP3, and B2M. Data were analysed by Kruskal-Wallis followed by Dunn's post hoc test. Placental weight and surface were increased in S-S and in D-D compared with P-P, whereas S-S and D-D were not different. No histological changes were observed among controls, but most genes had their expression decreased in P-P compared with S-S and D-D. The P-D foals had a 57% increased birthweight with heavier and larger placentas than P-P foals. The S-D foals were similar to both S-S and D-D in terms of birthweight and placental weight and surface. No major modifications in placental histology or transcript levels were observed in both enhanced groups. In contrast, S-P foals had a 37% decreased birthweight with lighter and smaller placentas compared with S-S and S-D foals. There was no gross histological difference between S-P and S-S but the microcotyledonary surface density was higher in S-P compared with S-D. Moreover, the expression of IGF2, IGF2R, SLC2A1, and eNOS was decreased in S-P compared with S-S. There was no difference in gene expression between S-P and P-P. In conclusion, intrauterine growth restriction led to marked changes in placental morphology, histology, and gene expression. The increased microcotyledonary surface density suggests a lengthening of villi, which could increase feto-maternal contact surface as a compensatory mechanism for the restricted uterine capacity. Surprisingly, placental adaptation to the restricted intrauterine environment in S-P induced gene profiles resembling that of control P, whereas no difference was observed in enhanced pregnancies.


2016 ◽  
Vol 79 (6) ◽  
pp. 821-830 ◽  
Author(s):  
Emily Cohen ◽  
Flora Y. Wong ◽  
Rosemary S.C. Horne ◽  
Stephanie R. Yiallourou

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