Enhanced Protein Levels of Protein Thiol/Disulphide Oxidoreductases in Placentae from Pre-eclamptic subjects

Shibata, Eiji; Ejima, Kuniaki; Nanri, Hiroki; Toki, Naoyuki; Koyama, Chiaki; Ikeda, Masaharu; Kashimura, Masamichi

doi:10.1053/plac.2001.0693

Cited by 59 publications

(34 citation statements)

References 26 publications

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“…PDI has a role in facilitating folding and export of secretory proteins from ER, and can also clear the toxic byproduct resulting from metabolism cell because of having structural protein similar to thioredoxin. Increased PDI in placentae from preeclamptic women has been reported that was in line with our observation [27] . An increase in the level of PDI has been shown as a response to ER injury [28] and oxidant stress.…”

Section: Discussionsupporting

confidence: 94%

Proteomic Analysis of Proteins Differentially Expressed in Preeclamptic Trophoblasts

Sun

Yang

et al. 2007

Gynecol Obstet Invest

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Aims: To identify differential trophoblastic proteins associated with preeclampsia (PE) by proteomic analysis. Methods: We isolated and purified placental trophoblasts from normotensive pregnant women and patients with PE by a continuous Percoll gradient. The expression of proteins was determined by sliver staining after two-dimensional polyacrylamide gel electrophoresis (2D-PAGE). Proteins of interest were identified using matrix-assisted laser desorption ionization time of flight mass spectrometry (MALDI-TOF-MS). Results: The overall trophoblastic protein expression patterns in preeclamptic and corresponding normotensive placentas were quite similar except for some areas. Of 34 differentially expressed protein spots (p < 0.05 by paired t-test), seven differential proteins from nine spots were identified by MALDI-TOF-MS. The expression of the following proteins was repressed (p < 0.01): disulfide isomerase ER-60, peroxiredoxin 2, and Δ3,5-Δ2,4-dienoyl-CoA isomerase. Four proteins (protein disulfide isomerase precursor, endoplasmic reticulum resident protein, dihydrolipoyl dehydrogenase and TIM21-like protein) were found to be significantly upregulated in PE (p < 0.01). Conclusion: We identified several proteins with significant altered expression in PE using 2D-PAGE. This method is a powerful technique with which to search for not only quantitative but also qualitative changes in a biological process of interest.

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Section: Discussionsupporting

confidence: 94%

Proteomic Analysis of Proteins Differentially Expressed in Preeclamptic Trophoblasts

Sun

Yang

et al. 2007

Gynecol Obstet Invest

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“…Interestingly, in preeclamptic placentas, which have abnormal placentation and increased oxidative stress, overexpression of the protein disulfide isomerase have been reported. 20 Moreover, our previously published data showed that protein disulfide isomerase was upregulated in the preeclamptic placentas. 17 GRP78 is a heat shock protein, which is recently characterized as p53 partner in trophoblast cells.…”

Section: Discussionmentioning

confidence: 97%

Proteome Differences in the First- and Third-Trimester Human Placentas

2015

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Placenta is a transient and unique pregnancy tissue that supports the fetus nutritionally and metabolically. Expression of the unique placental proteins in different stages may influence the development of the fetus as well as the pregnancy outcome. The present study aimed to compare the total placental proteome differences between the normal first-and third-trimester human placentas. In the current study, placental proteome was compared between normal first-and third-trimester placentas using 2-dimensional polyacrylamide gel electrophoresis method for separation and matrix-assisted laser desorption/ionization time-of flight mass spectrometry technique for identification of the proteins. Despite the overall similarities, comparison of the mean intensity of the protein spots between the first-and third-trimester placental proteomes revealed that 22 spots were differentially expressed (P < .05) among which 11 distinct spots were successfully identified. Of the 11 differentially expressed proteins, 4 were increased (protein disulfide isomerase, tropomyosin 4 isoform 2, enolase 1, and 78-kDa glucose-regulated protein), while the remaining 7 (actin g1 propeptide, heat shock protein gp96, a1-antitrypsin, EF-hand domain family member D1, tubulin a1, glutathione S-transferase, and vitamin D binding protein) showed decreased expression in the placentas from the first-trimester compared to the full-term ones. In summary, the results of the present study as the first research on the comparison of the first-and thirdtrimester human placental proteomes introduced a group of 11 proteins with altered expression. Interestingly, some of these proteins are reported to be altered in pregnancy-related disorders.

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“…The exact role of HNE in neurodegenerative disorders has yet to be established, but it is acknowledged that HNE is a highly toxic compound capable of causing neuronal cell death (58). We postulated that pretreatment of ALCAR+LA might protect neurons against HNEmediated oxidative stress.…”

Section: Discussionmentioning

confidence: 97%

Involvement of PI3K/PKG/ERK1/2 signaling pathways in cortical neurons to trigger protection by cotreatment of acetyl-L-carnitine and α-lipoic acid against HNE-mediated oxidative stress and neurotoxicity: Implications for Alzheimer's disease

Abdul

Butterfield

2007

Free Radical Biology and Medicine

126

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Oxidative stress has been shown to underlie neuropathological aspects of Alzheimer's disease (AD). 4-Hydroxy-2-nonenal (HNE) is a highly reactive product of lipid peroxidation of unsaturated lipids. HNE-induced oxidative toxicity is a well-described model of oxidative stress-induced neurodegeneration. GSH plays a key role in antioxidant defense, and HNE exposure causes an initial depletion of GSH that leads to gradual toxic accumulation of reactive oxygen species. In the current study, we investigated whether pre-treatment of cortical neurons with acetyl-L-carnitine (ALCAR) and α-lipoic acid (LA) plays a protective role in cortical neuronal cells against HNE-mediated oxidative stress and neurotoxicity. Decreased cell survival of neurons treated with HNE correlated with increased protein oxidation (protein carbonyl, 3-nitrotyrosine) and lipid peroxidation (HNE) accumulation. Pretreatment of primary cortical neuronal cultures with ALCAR and LA significantly attenuated HNE-induced cytotoxicity, protein oxidation, lipid peroxidation and apoptosis in a dosedependent manner. Additionally, pretreatment of ALCAR and LA also led to elevated cellular GSH and heat shock proteins (HSPs) levels compared to untreated control cells. We have also determined that pretreatment of neurons with ALCAR and LA leads to the activation of phosphoinositol-3 kinase (PI3K), PKG and ERK1/2 pathways, which play essential roles in neuronal cell survival. Thus, this study demonstrates a cross talk between the PI3K, PKG and ERK1/2 pathways in cortical neuronal cultures that contributes to ALCAR and LA-mediated pro-survival signaling mechanisms. This evidence supports the pharmacological potential of co-treatment of ALCAR and LA in the management of neurodegenerative disorders associated with HNE-induced oxidative stress and neurotoxicity, including AD.

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Enhanced Protein Levels of Protein Thiol/Disulphide Oxidoreductases in Placentae from Pre-eclamptic subjects

Cited by 59 publications

References 26 publications

Proteomic Analysis of Proteins Differentially Expressed in Preeclamptic Trophoblasts

Proteomic Analysis of Proteins Differentially Expressed in Preeclamptic Trophoblasts

Proteome Differences in the First- and Third-Trimester Human Placentas

Involvement of PI3K/PKG/ERK1/2 signaling pathways in cortical neurons to trigger protection by cotreatment of acetyl-L-carnitine and α-lipoic acid against HNE-mediated oxidative stress and neurotoxicity: Implications for Alzheimer's disease

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