Role of Oxidative Stress in Intrauterine Growth Restriction

2007 ◽  
Vol 64 (4) ◽  
pp. 187-192 ◽  
Author(s):  
Aydan Biri ◽  
Nuray Bozkurt ◽  
Ahmet Turp ◽  
Mustafa Kavutcu ◽  
Özdemir Himmetoglu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth

scholarly journals Oxidative Stress, Intrauterine Growth Restriction, and Developmental Programming of Type 2 Diabetes

Physiology ◽  
2018 ◽  
Vol 33 (5) ◽  
pp. 348-359 ◽  
Author(s):  
Cetewayo S. Rashid ◽  
Amita Bansal ◽  
Rebecca A. Simmons
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Intrauterine Growth Restriction ◽  
Metabolic Diseases ◽  
Growth Restriction ◽  
Mitochondria Dysfunction ◽  
Intrauterine Growth ◽  
And Oxidative Stress

Intrauterine growth restriction (IUGR) leads to reduced birth weight and the development of metabolic diseases such as Type 2 diabetes in adulthood. Mitochondria dysfunction and oxidative stress are commonly found in key tissues (pancreatic islets, liver, and skeletal muscle) of IUGR individuals. In this review, we explore the role of oxidative stress in IUGR-associated diabetes etiology.

Role of oxidative stress in preeclampsia and intrauterine growth restriction

2012 ◽  
Vol 38 (4) ◽  
pp. 658-664 ◽  
Author(s):  
Ismail Mert ◽  
Ayla Sargın Oruc ◽  
Serdar Yuksel ◽  
Esra Sukran Cakar ◽  
Umran Buyukkagnıcı ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Intrauterine Growth

scholarly journals Influence of Aerobic Training on the Reduced Vasoconstriction to Angiotensin II in Rats Exposed to Intrauterine Growth Restriction: Possible Role of Oxidative Stress and AT2 Receptor of Angiotensin II

PLoS ONE ◽  
2014 ◽  
Vol 9 (11) ◽  
pp. e113035 ◽  
Author(s):  
Vanessa Oliveira ◽  
Eliana Hiromi Akamine ◽  
Maria Helena C. Carvalho ◽  
Lisete Compagno Michelini ◽  
Zuleica Bruno Fortes ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Intrauterine Growth Restriction ◽  
Aerobic Training ◽  
Growth Restriction ◽  
At2 Receptor ◽  
Intrauterine Growth

The Role of the Anti-Angiogenic Factor Endostatin in Intrauterine Growth Restriction

2005 ◽  
Vol 12 (3) ◽  
pp. 195-197 ◽  
Author(s):  
Ariadne Malamitsi-Puchner ◽  
Theodora Boutsikou ◽  
Emmanuel Economou ◽  
Evangelos Makrakis ◽  
Zoe Iliodromiti ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Growth Restriction ◽  
Angiogenic Factor ◽  
Intrauterine Growth

The brain development of infants with intrauterine growth restriction: role of glucocorticoids

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Ying-xue Ding ◽  
Hong Cui
Keyword(s):  
Endothelial Cells ◽  
Brain Injury ◽  
Intrauterine Growth Restriction ◽  
Growth And Development ◽  
Growth Restriction ◽  
Microvascular Endothelial Cells ◽  
Intrauterine Growth ◽  
Growth Restrictions ◽  
The Brain

Abstract Brain injury is a serious complication of intrauterine growth restriction (IUGR), but the exact mechanism remains unclear. While glucocorticoids (GCs) play an important role in intrauterine growth and development, GCs also have a damaging effect on microvascular endothelial cells. Moreover, intrauterine adverse environments lead to fetal growth restriction and the hypothalamus-pituitary-adrenal (HPA) axis resetting. In addition, chronic stress can cause a decrease in the number and volume of astrocytes in the hippocampus and glial cells play an important role in neuronal differentiation. Therefore, it is speculated that the effect of GCs on cerebral neurovascular units under chronic intrauterine stimulation is an important mechanism leading to brain injury in infants with growth restrictions.

scholarly journals Label-Free Proteomics of the Fetal Pancreas Identifies Deficits in the Peroxisome in Rats with Intrauterine Growth Restriction

2019 ◽  
Vol 2019 ◽  
pp. 1-15
Author(s):  
Xiaomei Liu ◽  
Yanyan Guo ◽  
Jun Wang ◽  
Linlin Gao ◽  
Caixia Liu
Keyword(s):  
Oxidative Stress ◽  
Cell Cycle ◽  
Western Blotting ◽  
Proteomic Analysis ◽  
Intrauterine Growth Restriction ◽  
Bioinformatics Analysis ◽  
Growth Restriction ◽  
Label Free ◽  
Fetal Pancreas ◽  
Intrauterine Growth

Aim. The objective of the present study was to identify differentially expressed proteins (DEPs) in the pancreas of a fetus with intrauterine growth restriction (IUGR) and to investigate the molecular mechanisms leading to adulthood diabetes in IUGR. Methods. The IUGR rat model was induced by maternal protein malnutrition. The fetal pancreas was collected at embryonic day 20 (E20). Protein was extracted, pooled, and subjected to label-free quantitative proteomic analysis. Bioinformatics analysis (GO and IPA) was performed to define the pathways and networks associated with DEPs. LC-MS results were confirmed by western blotting and/or quantitative PCR (q-PCR). The principal parameters of oxidative stress-superoxide dismutase (Sod) were determined in blood samples of fetal rats. Results. A total of 57 DEPs (27 upregulated, 30 downregulated) were identified with a 1.5-fold change threshold and a p value ≤ 0.05 between the IUGR and the control pancreas. Bioinformatics analysis revealed that these proteins play important roles in peroxisome biogenesis and fission, fatty acid beta-oxidation (FAO), mitotic cell cycle, and histone modification. The peroxin Pex14 was downregulated in the IUGR pancreas as confirmed by western blotting and q-PCR. Pmp70, a peroxisomal membrane protein involved in the transport of fatty acids, was upregulated. Hsd17b4 and Acox1/2, which catalyze different steps of peroxisomal FAO, were dysregulated. Sod plasma concentrations in the IUGR fetus were higher than those in the control, suggesting partial compensation for oxidative stress. Multiple DEPs were related to the regulation of the cell cycle, including reduced Cdk1, Mcm2, and Brd4. The histone acetylation regulators Hdac1/2 were downregulated, whereas Sirt1/3 and acetylated H3K56 were increased in the IUGR fetal pancreas. Conclusion. The present study identified DEPs in the fetal pancreas of IUGR rats by proteomic analysis. Downregulation of pancreas peroxins and dysregulation of enzymes involved in peroxisomal FAO may impair the biogenesis and function of the peroxisome and may underlie the development of T2 diabetes mellitus in adult IUGR rats. Disorders of cell cycle regulators may induce cell division arrest and lead to smaller islets. The present data provide new insight into the role of the peroxisome in the development of the pancreas and may be valuable in furthering our understanding of the pathogenesis of IUGR-induced diabetes.

Angiopoietin-2 in the perinatal period and the role of intrauterine growth restriction

2006 ◽  
Vol 85 (1) ◽  
pp. 45-48 ◽  
Author(s):  
Ariadne Malamitsi-Puchner ◽  
Theodora Boutsikou ◽  
Emmanuel Economou ◽  
Anastasia Tzonou ◽  
Evangelos Makrakis ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Perinatal Period ◽  
Growth Restriction ◽  
Intrauterine Growth ◽  
Angiopoietin 2

scholarly journals The detrimental role of angiotensin receptor agonistic autoantibodies in intrauterine growth restriction seen in preeclampsia

2009 ◽  
Vol 206 (12) ◽  
pp. 2809-2822 ◽  
Author(s):  
Roxanna A. Irani ◽  
Yujin Zhang ◽  
Sean C. Blackwell ◽  
Cissy Chenyi Zhou ◽  
Susan M. Ramin ◽  
...  
Keyword(s):  
Intrauterine Growth Restriction ◽  
Causative Factor ◽  
Growth Restriction ◽  
Hypertensive Disorder ◽  
Human Trophoblast ◽  
Fetal Circulation ◽  
Intrauterine Growth ◽  
Underlying Mechanisms ◽  
Agonistic Autoantibodies

Growth-restricted fetuses are at risk for a variety of lifelong medical conditions. Preeclampsia, a life-threatening hypertensive disorder of pregnancy, is associated with fetuses who suffer from intrauterine growth restriction (IUGR). Recently, emerging evidence indicates that preeclamptic women harbor AT1 receptor agonistic autoantibodies (AT1-AAs) that contribute to the disease features. However, the exact role of AT1-AAs in IUGR and the underlying mechanisms have not been identified. We report that these autoantibodies are present in the cord blood of women with preeclampsia and retain the ability to activate AT1 receptors. Using an autoantibody-induced animal model of preeclampsia, we show that AT1-AAs cross the mouse placenta, enter fetal circulation, and lead to small fetuses with organ growth retardation. AT1-AAs also induce apoptosis in the placentas of pregnant mice, human villous explants, and human trophoblast cells. Finally, autoantibody-induced IUGR and placental apoptosis are diminished by either losartan or an autoantibody-neutralizing peptide. Thus, these studies identify AT1-AA as a novel causative factor of preeclampsia-associated IUGR and offer two possible underlying mechanisms: a direct detrimental effect on fetal development by crossing the placenta and entering fetal circulation, and indirectly through AT1-AA–induced placental damage. Our findings highlight AT1-AAs as important therapeutic targets.

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