99 THE DIFFERENTIAL EXPRESSION OF CALCIUM-RELATED PROTEINS BY HYPOXIC STRESS IN THE DUODENUM, KIDNEY, AND PLACENTA OF PREGNANT RATS

2013 ◽  
Vol 25 (1) ◽  
pp. 197
Author(s):  
H. Yang ◽  
E. B. Jeung
Keyword(s):  
Oxidative Stress ◽  
De Novo ◽  
Hypoxic Condition ◽  
First Trimester ◽  
Rat Tissues ◽  
Hypoxic Stress ◽  
Pregnant Rats ◽  
Extracellular Sodium ◽  
Related Proteins ◽  
And Oxidative Stress

Preeclampsia is a pregnancy-specific disease characterized by the de novo development of concurrent hypertension, proteinuria, and oxidative stress in placenta. Hypoxia occurs during the development of placenta in the first trimester and is implicated in trophoblast differentiation. Oxidative stress, resulting from deficient remodeling of spiral arteries, is an important inducer of preeclampsia. The potassium-dependent sodium/calcium exchangers including NCKX3 and NCX1 play critical roles in the transport of intracellular calcium that is exchanged with extracellular sodium ions. Calcium-related proteins, NCXs, calbindin, calcium pumping proteins (TRPV5-6, PMCA1b), transcripts are abundant in the smooth muscle, uterus, aorta, and intestine. The expressions of calcium-related proteins in the kidney, duodenum, and placenta after hypoxic stress in rats at gestation Day 19.5 (GD 19.5) were examined by real-time PCR and Western blot analysis. Hypoxic condition did not change fetal weight; however, it significantly increased the weight of placenta compared to normoxic condition. In GD 19.5, renal NCKX3 and TRPV6 expressions were increased, whereas the levels of NCX1 were decreased in hypoxic rats compared with normoxic pregnant rats. The expressions of CaBP-9k, TRPV5, and PMCA1b were not altered in normoxic or hypoxic rat tissues. Duodenal expressions of CaBP-9k, TRPV5-6, and PMCA1 were decreased in hypoxic rats, whereas NCXs were not changed. The transcripts of NCKX3, TRPV5-6, and PMCA1b were highly expressed in the placenta of hypoxic rat. Taken together, the expressions of renal, duodenal, and placental calcium-related proteins appear to be modulated by hypoxia-induced oxidative stress, implying that calcium-related proteins may be involved in preeclamptic oxidative stress.

81 MEMBRANE AND CYTOSOLIC CALCIUM PROTEINS, TRPV6, PMCA1, NCKX3, NCX1 AND CaBP-28k, APPEAR TO BE DISTINCTLY REGULATED IN HUMAN CHORIOCARCINOMA AND PLACENTAL CELLS

2012 ◽  
Vol 24 (1) ◽  
pp. 153 ◽  
Author(s):  
E. B. Jeung ◽  
H. Yang
Keyword(s):  
Oxidative Stress ◽  
De Novo ◽  
Hormone Secretion ◽  
First Trimester ◽  
Cytosolic Calcium ◽  
Primary Cell ◽  
Bewo Cell ◽  
Hypoxic Stress ◽  
Multiple Comparison Test ◽  
Protein Expressions

Preeclampsia is a pregnancy-specific disease characterised by de novo development of concurrent hypertension, proteinuria and oxidative stress in the placenta. In the placenta, intervillous blood flow increases after 10 weeks of gestation and results in exposure of trophoblast cells to oxygen. Hypoxia occurs during the development of placenta in the first trimester and is implicated in trophoblast differentiation. Ca2+ is a universal intracellular second messenger involved in many processes such as signal transduction, hormone secretion and programmed cell death. Human placental primary cell cultures were established from first-trimester human placentas (at 7 to 12 weeks of gestation). In this study, calcium-related proteins (CRPs; TRPV6, PMCA1, NCKX3 and CaBP-28k) were investigated at normoxia (5% CO2 in 95% air) or hypoxia (2% O2/93% N2/5%CO2) for 12 h in human placental cell line (BeWo) and human placental primary cell (hPC). We confirmed mRNA expression by real-time PCR and protein expression by Western blot analysis. The data were 2 or 3 individual experiments with triplicate samples and analysed by one-way ANOVA using Tukey's multiple comparison test. In hypoxia, the level of TRPV6 mRNA and protein was not changed, however, calcium transporters' (NCKX3, CaBP-28k) mRNA and protein expressions were significantly increased in hypoxic BeWo cell compared with control (normoxia). In addition, expression of PMCA1 mRNA and protein was decreased in hypoxic BeWo cells. In hPC, CRPs (TRPV6, PMCA1, NCKX3 and CaBP-28k) mRNA and protein expressions were significantly induced by hypoxic stress compared with control. These results, taken together, indicate that alterations of calcium transporters in hypoxic stress may be involved in calcium transport in the placenta and protection of the placental trophoblasts from the oxidative stress during the pregnancy.

scholarly journals Amino Acid Transporter LAT1 (SLC7A5) Mediates MeHg-Induced Oxidative Stress Defense in the Human Placental Cell Line HTR-8/SVneo

2021 ◽  
Vol 22 (4) ◽  
pp. 1707
Author(s):  
Sebastian Granitzer ◽  
Raimund Widhalm ◽  
Martin Forsthuber ◽  
Isabella Ellinger ◽  
Gernot Desoye ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acid ◽  
De Novo ◽  
Structural Similarity ◽  
Amino Acid Transporter ◽  
Cell Number ◽  
Mehg Exposure ◽  
Acid Transporter ◽  
And Oxidative Stress

The placental barrier can protect the fetus from contact with harmful substances. The potent neurotoxin methylmercury (MeHg), however, is very efficiently transported across the placenta. Our previous data suggested that L-type amino acid transporter (LAT)1 is involved in placental MeHg uptake, accepting MeHg-L-cysteine conjugates as substrate due to structural similarity to methionine. The aim of the present study was to investigate the antioxidant defense of placental cells to MeHg exposure and the role of LAT1 in this response. When trophoblast-derived HTR-8/SVneo cells were LAT1 depleted by siRNA-mediated knockdown, they accumulated less MeHg. However, they were more susceptible to MeHg-induced toxicity. This was evidenced in decreased cell viability at a usually noncytotoxic concentration of 0.03 µM MeHg (~6 µg/L). Treatment with ≥0.3 µM MeHg increased cytotoxicity, apoptosis rate, and oxidative stress of HTR-8/SVneo cells. These effects were enhanced under LAT1 knockdown. Reduced cell number was seen when MeHg-exposed cells were cultured in medium low in cysteine, a constituent of the tripeptide glutathione (GSH). Because LAT1-deficient HTR-8/SVneo cells have lower GSH levels than control cells (independent of MeHg treatment), we conclude that LAT1 is essential for de novo synthesis of GSH, required to counteract oxidative stress. Genetic predisposition to decreased LAT1 function combined with MeHg exposure could increase the risk of placental damage.

Dynamics of inflammatory reaction and oxidative stress across maternal serum, placenta and amniotic fluid in laboratory rats and the role played by genistein aglycone

2018 ◽  
Vol 30 (1) ◽  
pp. 37-45 ◽  
Author(s):  
Funmileyi O. Awobajo ◽  
Ayodele O. Morakinyo ◽  
Titilola A. Samuel ◽  
Oluwakemi T. Oyelowo ◽  
Abimbola O. Ogunsola ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amniotic Fluid ◽  
Inflammatory Reaction ◽  
Corticosterone Level ◽  
Maternal Serum ◽  
Late Gestation ◽  
Oxidative Stress Biomarkers ◽  
Pregnant Rats ◽  
Hsp90 Level ◽  
And Oxidative Stress

Abstract Background Genistein was reported to adversely influence fetal development although this is yet to be fully understood as a mechanism. Methods In this study, pregnant rats were divided into control (Cont.) and genistein force-fed (2-mg/kg and 4-mg/kg) groups. Each group was divided further into five subgroups: GD-0, GD-6, GD-13, GD-18, and GD-20 based on the terminal gestational day (GD). On the respective terminal GD, the rats were sacrificed and blood samples and amniotic fluid were carefully collected and separated and placenta homogenates were prepared. These samples were evaluated for oxidative stress and inflammatory reaction. The weights of embryonic implant and placenta tissue were also recorded. Heat shock protein (Hsp) (60 and 90), corticosterone, and oxidative stress biomarkers were determined in all the samples. Results Fetal and placental weights in all genistein-exposed groups were significantly decreased. A fluctuation in the level of the Hsp was recorded with a significant decrease recorded in Hsp90 level in the placenta and amniotic fluid towards GD-20 along with a concomitant increase in the corticosterone level in the amniotic fluid in all genistein groups compared to control. Maternal serum at GD-18 and GD -20 recorded a significant increase in antioxidant level (SOD, GSH, CAT) in all genistein-exposed groups. However, these antioxidants were significantly reduced in the placenta and the amniotic fluid compared to control. Conclusions Genistein enhances the placenta function in attenuating the risk of oxidative stress in the amniotic fluid and deferentially suppressed inflammatory activities in the placenta during early gestation and towards late gestation period.

Woman's body symmetry and oxidative stress in the first trimester of pregnancy

2015 ◽  
Vol 27 (6) ◽  
pp. 816-821 ◽  
Author(s):  
Agnieszka Żelaźniewicz ◽  
Judyta Nowak ◽  
Bogusław Pawłowski
Keyword(s):  
Oxidative Stress ◽  
First Trimester ◽  
First Trimester Of Pregnancy ◽  
And Oxidative Stress ◽  
Woman's Body

Ergosterol attenuates cigarette smoke extract-induced COPD by modulating inflammation, oxidative stress and apoptosis in vitro and in vivo

2019 ◽  
Vol 133 (13) ◽  
pp. 1523-1536 ◽  
Author(s):  
Xiao Sun ◽  
Xiuli Feng ◽  
Dandan Zheng ◽  
Ang Li ◽  
Chunyan Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cigarette Smoke ◽  
Cigarette Smoke Extract ◽  
Cordyceps Sinensis ◽  
Chronic Obstructive ◽  
Therapeutic Effects ◽  
Related Proteins ◽  
And Oxidative Stress

Abstract Cigarette smoke (CS) is the major cause of chronic obstructive pulmonary disease (COPD). CS heightens inflammation, oxidative stress and apoptosis. Ergosterol is the main bioactive ingredient in Cordyceps sinensis (C. sinensis), a traditional medicinal herb for various diseases. The objective of this work was to investigate the effects of ergosterol on anti-inflammatory and antioxidative stress as well as anti-apoptosis in a cigarette smoke extract (CSE)-induced COPD model both in vitro and in vivo. Our results demonstrate that CSE induced inflammatory and oxidative stress and apoptosis with the involvement of the Bcl-2 family proteins via the nuclear factor kappa B (NF-κB)/p65 pathway in both 16HBE cells and Balb/c mice. CSE induced epithelial cell death and increased the expression of nitric oxide (NO), interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), malondialdehyde (MAD) and the apoptosis-related proteins cleaved caspase 3/7/9 and cleaved-poly-(ADP)-ribose polymerase (PARP) both in vitro and in vivo, whereas decreased the levels of superoxide dismutase (SOD) and catalase (CAT). Treatment of 16HBE cells and Balb/c mice with ergosterol inhibited CSE-induced inflammatory and oxidative stress and apoptosis by inhibiting the activation of NF-κB/p65. Ergosterol suppressed apoptosis by inhibiting the expression of the apoptosis-related proteins both in vitro and in vivo. Moreover, the usage of QNZ (an inhibitor of NF-κB) also partly demonstrated that NF-κB/p65 pathway was involved in the ergosterol protective progress. These results show that ergosterol suppressed COPD inflammatory and oxidative stress and apoptosis through the NF-κB/p65 pathway, suggesting that ergosterol may be partially responsible for the therapeutic effects of cultured C. sinensis on COPD patients.

Biomonitoring of the Genotoxic and Hepatotoxic Effects and Oxidative Stress Potentials of Itraconazole in Pregnant Rats

2015 ◽  
Vol 104 (2) ◽  
pp. 55-64 ◽  
Author(s):  
Abdel-Fattah El-Shershaby ◽  
Ahmed I. Dakrory ◽  
Mai H. El-Dakdoky ◽  
Jehane Ibrahim ◽  
Fatma Kassem
Keyword(s):  
Oxidative Stress ◽  
Pregnant Rats ◽  
And Oxidative Stress

scholarly journals Alterations in Energy Metabolism, Mitochondrial Function and Redox Homeostasis in GK Diabetic Rat Tissues Treated with Aspirin

Life ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 104
Author(s):  
Annie John ◽  
Layla Amiri ◽  
Jasmin Shafarin ◽  
Saeed Tariq ◽  
Ernest Adeghate ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Mitochondrial Function ◽  
Redox Homeostasis ◽  
Diabetic Rats ◽  
Endocrine Function ◽  
Diabetic Rat ◽  
Rat Tissues ◽  
Gk Rats ◽  
And Oxidative Stress

Our recent studies have demonstrated that aspirin treatment prevents inflammatory and oxidative stress-induced alterations in mitochondrial function, improves glucose tolerance and pancreatic endocrine function and preserves tissue-specific glutathione (GSH)-dependent redox homeostasis in Goto-Kakizaki (GK) diabetic rats. In the current study, we have investigated the mechanism of action of aspirin in maintaining mitochondrial bioenergetics and redox metabolism in the liver and kidneys of GK rats. Aspirin reduced the production of reactive oxygen species (ROS) and oxidative stress-induced changes in GSH metabolism. Aspirin treatment also improved mitochondrial respiratory function and energy metabolism, in addition to regulating the expression of cell signaling proteins that were altered in diabetic animals. Ultrastructural electron microscopy studies revealed decreased accumulation of glycogen in the liver of aspirin-treated diabetic rats. Hypertrophic podocytes with irregular fusion of foot processes in the renal glomerulus and detached microvilli, condensed nuclei and degenerated mitochondria observed in the proximal convoluted tubules of GK rats were partially restored by aspirin. These results provide additional evidence to support our previous observation of moderation of diabetic complications by aspirin treatment in GK rats and may have implications for cautious use of aspirin in the therapeutic management of diabetes.

scholarly journals Resveratrol inhibits autophagy in HTR-8/SVneo model by alleviating trophoblast oxidative stress

2020 ◽  
Author(s):  
Meihe LI ◽  
Minchao KANG ◽  
Peng AN ◽  
Huimin DANG ◽  
Xin XU
Keyword(s):  
Oxidative Stress ◽  
First Trimester ◽  
Normal Function ◽  
Beclin 1 ◽  
Extravillous Trophoblast ◽  
Successful Outcome ◽  
Beneficial Effects ◽  
Vitro Model ◽  
Related Proteins

Abstract BackgroundThe normal function of the placenta at each time stage of pregnancy is essential to a successful outcome. Placental dysfunction and increased oxidative stress and autophagy are the cause of a series of severe pregnancy complications. Resveratrol is a potent antioxidant that has shown beneficial effects in many diseases. We aim to investigate whether excessive autophagy is associated with oxidative stress in the trophoblast oxidative stress model. Resveratrol was taken to clarify its role in excessive autophagy of placental trophoblasts. MethodsWe established an in vitro model of oxidative stress by exposing the human first-trimester extravillous trophoblast cell line HTR-8/SVneo to H2O2. Levels of autophagy-related proteins (LC3, Beclin-1, p53 and mTOR) were detected by western blot.ResultsTreatment with resveratrol significantly ameliorated H2O2-induced cytotoxicity, morphological damage, oxidative stress and autophagy. Mechanistically, resveratrol restored the levels of autophagy-related proteins including LC3-II, Beclin-1 and p53, mTOR that were dysregulated by H2O2.ConclusionsResveratrol may protect human trophoblasts against H2O2-induced oxidative stress by reducing excessive autophagy, thus ensuring the normal biological functions of trophoblasts.

scholarly journals Kynurenine Metabolism Lifespan Extension Mediated by Oxidative Stress Response and Hypoxic Response in C. elegans

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 684-684
Author(s):  
Raul Castro-Portuguez ◽  
Jeremy Meyers ◽  
Sam Freitas ◽  
Hope Dang ◽  
Emily Turner ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factors ◽  
Stress Response ◽  
Aging Process ◽  
De Novo ◽  
Kynurenine Pathway ◽  
Oxidative Stress Response ◽  
Lifespan Extension ◽  
Hypoxic Stress ◽  
C Elegans

Abstract Aging is characterized by a progressive decline in the normal physiological functions of an organism, ultimately leading to mortality. Metabolic changes throughout the aging process disrupt the balance and homeostasis of the cell. The kynurenine metabolic pathway is the sole de novo biosynthetic pathway for producing NAD+ from ingested tryptophan. Altered kynurenine pathway activity is associated with both aging and a variety of age-associated diseases, and kynurenine-based interventions can extend lifespan in Caenorhabditis elegans. Our laboratory recently demonstrated knockdown of the kynurenine pathway enzymes kynureninase (KYNU) or 3-hydroxyanthranilic acid dioxygenase (HAAO) increases lifespan by 20-30% in C elegans. However, the mechanism of how these interventions may modulate response against different stressors during the aging process has yet to be explored. Fluorescent reporter strains show the stress-responsive transcription factors skn-1 (ortholog of NRF2/NFE2L2; oxidative stress response) and hif-1 (ortholog of HIF1A; hypoxic stress response) to be highly upregulated when the kynurenine pathway is inhibited. We also demonstrated the increase expression of gst-4 and gcs-1 (transcriptional targets skn-1), which are involved in production of the antioxidant glutathione (GSH), as well as upregulation of cysl-2 (transcriptional target of hif-1), a regulator of cysteine biosynthesis from serine. We hypothesize that lifespan extension resulting from kynurenine pathway inhibition is mediated, at least in part, by upregulation of these transcription factors, providing elevated defense against oxidative stress and hypoxic stress.

scholarly journals Magnesium Lithospermate B Downregulates the Levels of Blood Pressure, Inflammation, and Oxidative Stress in Pregnant Rats with Hypertension

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Kaixiang Xu ◽  
Xiaohong Zang ◽  
Mian Peng ◽  
Qian Zhao ◽  
Binbin Lin
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Gestational Hypertension ◽  
Protective Effects ◽  
Urine Protein ◽  
Pregnant Rats ◽  
Protein Levels ◽  
Arterial Blood ◽  
Magnesium Lithospermate B ◽  
And Oxidative Stress

Background. Magnesium lithospermate B (MLB) was shown to suppress oxidative stress and reduce hypertension, but the role of MLB in pregnancy-induced hypertension (PIH) remains unknown. The objective of this study was to demonstrate the effects of MLB on rats with PIH. Methods. A total of 40 pregnant SD rats were selected, and 30 rats were orally given NG-nitro-L-arginine methyl ester (L-NAME, 60 mg/kg/day) to establish PIH rat models. Rats were equally divided into four groups: control, PIH, 5 mg/kg MLB, and 10 mg/kg MLB. MLB was consecutively administered into PIH rats for one week. The effects of MLB on mean arterial blood pressure (MAP), urine protein level, inflammation, and oxidative stress together with angiogenesis were analyzed. Results. MLB prevented the elevation in MAP and urine protein levels induced by L-NAME. The activities of inflammatory cytokines were highly increased in serum and placental tissues of PIH rats, while cotreatment with MLB partially reversed the activities of these cytokines. MLB also recovered the expression of reactive oxygen species (ROS) in plasma of PIH rats together with levels of oxidative stress and antioxidant capacity in the placenta of PIH rats. The decreased expressions of vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), and NO observed in PIH rats were increased by MLB. In addition, 10 mg/kg MLB exhibited higher protective effects as compared to lower doses of 5 mg/kg. Conclusion. This study demonstrated that pretreatment with MLB decreased MAP, inflammation, and oxidative stress in rats with gestational hypertension.

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