mRNA expression and protein localization of placental tissue proteins in malignant tumors

Placenta ◽  
1995 ◽  
Vol 16 (7) ◽  
pp. A19
Author(s):  
Tamaki Yudate ◽  
Yoshichika Suzuki ◽  
Keiichi Isaka ◽  
Junko Takada ◽  
Makoto Hosaka ◽  
...  
2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Travis Alvine ◽  
Archana Dhasarathy ◽  
Amy Bundy ◽  
Atrayee Bhattacharya ◽  
Diane Darland ◽  
...  

Abstract Objectives The maternal diet and obesity adversely affect placental structure/function, inflammation, and alters placental DNA methylation. RNA-binding motif single-stranded interacting protein 1 (RBMS1) regulates DNA replication and gene transcription and is expressed in the placenta. Although specific roles for RBMS1 in the context of obesity have not yet been fully explored, RBMS1 has been linked to type 2 diabetes mellitus risk. No data are available regarding the function of RBMS1 in placental tissue and whether placental expression of RBMS1 is regulated differentially in obesity. Methods Placental tissue from obese (BMI > 25, n = 15) and non-overweight (BMI < 25, n = 3) women was obtained from The Cooperative Human Tissue Network (CHTN) Western Division at Vanderbilt University Medical Center. Epigenetic changes in placental RBMS1 DNA methylation and histone acetylation were assessed by DNA methylation assays and chromatin immunoprecipitation, respectively. Placental RBMS1 gene expression was measured by RT-PCR and RBMS1 protein localization was assessed by immunohistochemistry. The anti-inflammatory effect of RBMS1 was measured in vitro using human placental fibroblast cells (HS 795.PI). Placental short-chain fatty acids (SCFAs) were measured by gas chromatography-mass spectrometry (GC-MS). Results RBMS1 mRNA (P = 0.0029) and DNA methylation (P < 0.05) were increased in placentae from obese mothers. RBMS1 protein expression was localized to placental resident macrophages and fibroblastic cells. In vitro, RBMS1 recombinant protein attenuated LPS-induced IL-6 mRNA expression in HS 795.PI cells (P < 0.001), suggesting a possible anti-inflammatory role for RBMS1 in the context of placental inflammation. SCFA analysis demonstrated an increase in placental butyrate (P = 0.0327), a known histone deacetylase (HDAC) inhibitor in placenta from obese women. Conclusions These data suggest a possible anti-inflammatory role for RBMS1 in the context of placental inflammation. Increased placental RBMS1 expression in obese women may serve as an adaptive response to reduce placental inflammation. Funding Sources USDA Agricultural Research Service Project #3062-51000-052-00D.


2009 ◽  
Vol 84 (1) ◽  
pp. 68-75 ◽  
Author(s):  
Beata Telejko ◽  
Mariusz Kuzmicki ◽  
Anna Zonenberg ◽  
Jacek Szamatowicz ◽  
Natalia Wawrusiewicz-Kurylonek ◽  
...  

2001 ◽  
pp. 187-192 ◽  
Author(s):  
E Schoof ◽  
M Girstl ◽  
W Frobenius ◽  
M Kirschbaum ◽  
R Repp ◽  
...  

BACKGROUND: During human pregnancy, 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays an important role in protecting the fetus from high maternal glucocorticoid concentrations by converting cortisol to inactive cortisone. Furthermore, 11beta-HSD2 is indirectly involved in the regulation of the prostaglandin inactivating enzyme 15-hydroxyprostaglandin dehydrogenase (PGDH), because cortisol reduces the gene expression and enzyme activity of PGDH in human placental cells. OBJECTIVE: To examine developmental changes in placental 11beta-HSD2 and PGDH gene expression during the 2nd and 3rd trimesters of human pregnancies. METHODS: In placental tissue taken from 20 healthy women with normal pregnancy and 20 placentas of 17 mothers giving birth to premature babies, 11beta-HSD2 and PGDH mRNA expression was determined using quantitative real-time PCR. RESULTS: Placental mRNA expression of 11beta-HSD2 and PGDH increased significantly with gestational age (r=0.55, P=0.0002 and r=0.42, P=0.007). In addition, there was a significant correlation between the two enzymes (r=0.58, P<0.0001). CONCLUSIONS: In the course of pregnancy there is an increase in 11beta-HSD2 and PGDH mRNA expression in human placental tissue. This adaptation of 11beta-HSD2 prevents increasing maternal cortisol concentrations from transplacental passage and is exerted at the gene level. 11beta-HSD2 up-regulation may also lead to an increase in PGDH mRNA concentrations that, until term, possibly delays myometrial contractions induced by prostaglandins.


2012 ◽  
Vol 214 (1) ◽  
pp. 79-85 ◽  
Author(s):  
Judith E Cartwright ◽  
Paula Juliet Williams

Kisspeptin, originally identified as metastatin, important in preventing cancer metastasis, has more recently been shown to be important in pregnancy. Roles indicated for kisspeptin in pregnancy include regulating trophoblast invasion and migration during placentation. The pregnancy-specific disorder pre-eclampsia (PE) is now accepted to begin with inadequate trophoblast invasion and the current study therefore sets out to characterise placental expression of both kisspeptin (KISS1) and its receptor (KISS1R) throughout pregnancy and in PE. Placental tissue was obtained from women undergoing elective surgical termination of early pregnancy (n=10) and from women following Caesarean section at term in normal pregnancy (n=10) and with PE (n=10). Immunohistochemistry of paraffin embedded sections and western immunoblotting were performed to assess protein localisation and expression. Quantitative real-time PCR was carried out to evaluate mRNA expression of both KISS1 and KISS1R. Protein and mRNA expression was found to mirror each other with KISS1 expression found to be reduced in PE compared with that in normal term pregnancy. Interestingly, KISS1R expression at both the mRNA and protein levels was found to be increased in PE compared with that in normal term pregnancy. The current findings of increased KISS1R expression may represent a mechanism by which functional activity of KISS1 is higher in PE than in normal pregnancy. Higher levels of activity of KISS1R may be involved in inhibition of trophoblast invasion and angiogenesis, which are associated with PE.


2009 ◽  
Vol 390 (11) ◽  
Author(s):  
Stephanie Pildner von Steinburg ◽  
Achim Krüger ◽  
Thorsten Fischer ◽  
Karl-Theodor Mario Schneider ◽  
Manfred Schmitt

AbstractIn preeclampsia and hemolysis, elevated liver enzymes and low platelet (HELLP) syndrome, impaired trophoblast invasion and excessive fibrin deposition in the placental intervillous space is associated with fetal compromise. However, little information is available whether modulation of placental protease expression – potentially causing impaired trophoblast invasion – is associated with the HELLP syndrome. Total RNA and protein were extracted from placental tissue from 11 females with HELLP syndrome and 8 controls matched for gestational age. mRNA expression of matrix metalloprotease (MMP) -2 and -9, tissue inhibitors of metalloprotease (TIMP) -1, -2, and -3, and urokinase-type plasminogen activator receptor (uPAR) was determined by Northern blotting. Protein expression of MMP-2 and -9, and TIMP-1 and -2 was detected by Western blotting and that of uPA, uPAR, and plasminogen activator inhibitor (PAI) -1 by ELISA. In patients with HELLP syndrome, mRNA expression of MMP-2 and TIMP-2 was decreased, whereas TIMP-1 and -3 levels were unchanged. MMP-9 and uPAR mRNA was undetectable in both groups. Protein expression of all investigated proteolytic factors remained unchanged. Our findings at the mRNA level suggest a decrease in matrix remodeling in placentae from patients with HELLP syndrome compared with control pregnancies, although this is not supported at the protein level.


1999 ◽  
Vol 86 (1) ◽  
pp. 313-319 ◽  
Author(s):  
Pamela Mitchell ◽  
Tom Steenstrup ◽  
Kevin Hannon

The potential role of the fibroblast growth factor (FGF) family during stretch-induced postnatal skeletal muscle hypertrophy was analyzed by using an avian wing-weighting model. After 2 or 11 days of weighted stretch, anterior latissimus dorsi (ALD) muscles were, on average, 34 ( P < 0.01) and 85% ( P < 0.01) larger, respectively, than unweighted ALD control muscles. By using quantitative RT-PCR, FGF-1 mRNA expression was found to be significantly decreased in ALD muscles stretched for 2 or 11 days. In contrast, FGF-4 and FGF-10 mRNA expression was significantly increased 2 days after initiation of stretch. FGF-2, FGF-10, fibroblast growth factor receptor 1, and FREK mRNA expression was significantly increased at 11 days poststretch. Increases in FGF-2 and FGF-4 protein could be detected throughout the myofiber periphery after 11 days of stretch. On a cellular level, FGF-2 and FGF-4 proteins were differentially localized. This differential expression pattern and protein localization of the FGF family in response to stretch-induced hypertrophy suggest distinct roles for individual FGFs during the postnatal hypertrophy process.


Placenta ◽  
1993 ◽  
Vol 14 (4) ◽  
pp. A31
Author(s):  
Keiichi Isaka ◽  
Yoshichika Suzuki ◽  
Tamaki Yudate ◽  
Makoto Koshiishi ◽  
Shizuko Yamabe ◽  
...  

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 729-729
Author(s):  
Luisa Castillo ◽  
Katherine Delaney ◽  
Ronnie Guillet ◽  
Eva Pressman ◽  
Kimberly O'Brien

Abstract Objectives Our objective was to evaluate placental EPO mRNA expression in term and preterm placentae and explore maternal/neonatal/placental determinants of EPO expression. Methods Placental tissue was collected from pregnant adolescents (n = 82, &lt; 19 y of age) and from women (n = 62) carrying multiple fetuses (twins = 23, triplets = 39). Placental mRNA expression was evaluated using qPCR. Hemoglobin and iron status biomarkers (SF, TBI, sTfR, Hepcidin) were measured in maternal blood at delivery and in cord blood. Results In this population, women delivered between 30–42 weeks of gestation. Of the 144 women, 30% delivered prematurely (&lt; 37 weeks, n = 44) and 69% delivered at term (≥37 weeks, n = 100). As expected, preterm placentae weighed significantly less than term placenta (293 ± 93 g vs. 544 ± 143 g, p &lt; 0.0001). Placental EPO mRNA expression was detected in all samples collected. Placental EPO mRNA expression did not significantly differ between anemic (Hb &lt; 13 g/dL) (n = 23) and non-anemic (n = 84) neonates (p = 0.69), nor was it significantly associated with maternal anemia at delivery (p = 0.44). Placental EPO mRNA expression was also not significantly associated with maternal (p = 0.56) or neonatal (p = 0.61) Hb concentrations, placental weight (p = 0.46) or gestational age at delivery (p = 0.39). Conclusions While placental EPO mRNA was detected in all placental tissue collected between 30–42 weeks of gestation none of the iron biomarkers evaluated were significantly related to placental EPO mRNA expression. Further studies are needed to understand determinants of placental EPO mRNA and protein expression. Funding Sources The U.S. National Institutes of Health (NIH) National Institute of Child Health and Development (NICHD) Grant 1R21HD098864, The Gerber Foundation and USDA grants 2005–35,200-15,218 and 2009–35,200-05,171.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1024-1024
Author(s):  
Kate Larson ◽  
Amy Bundy ◽  
James Roemmich

Abstract Objectives We have shown that male offspring (F1) of fathers (F0) fed a high fat (HF) diet and exercised had greater skeletal muscle insulin signaling and reduced T2DM risk compared to fathers fed HF diet and remain sedentary. The current study extends this work by hypothesizing that F0 HF diet and exercise regulate F1 T2DM risk by early alterations in epigenetics of placental tissue growth via changes in sperm miRNA expression. Methods To test these hypotheses, three-week old male C57BL/6 mice were fed a normal-fat (NF) diet (16% fat) or a HF diet (45% fat) and assigned to either voluntary wheel running exercise or cage activity for 3 months prior to mating with NF diet fed dams. F0 sperm and placental tissue samples were collected to determine changes in placental and fetal weights, placental gene expression, and F0 sperm miRNA expression. Results F0 sperm miRNA 193b expression was decreased while miRNA 204 was increased by paternal exercise. Protein expression of di-methylated histone 3 lysine 9 was decreased with F0 HF diet. Placental and fetal tissue weights were decreased by F0 HF diet in F1 males while no changes in the F1 females. Placental proinflammatory cytokine mRNA expression, including IL-1 beta and TNF-alpha, was reduced by paternal exercise while nutrient transporter mRNA expression was decreased by paternal HF diet only in the placentae of F1 females. Treatment of primary placental cell with miRNA 193 inhibited TNF-alpha mRNA expression. In addition, treatment of the same cells with TNF-alpha increased SLC6a19. Moreover, paternal exercise increased body weight at weaning in a female offspring. Conclusions These results demonstrate that placental tissue weight, placental nutrient transporter gene expression and fetal weights are altered by paternal exercise while placental inflammatory gene expression are influenced by paternal exercise in offspring in a sex-specific manner. Funding Sources This work was supported by USDA ARS Project #3062–51,000-054–00D.


1991 ◽  
Vol 75 (3) ◽  
pp. 447-451 ◽  
Author(s):  
Timothy B. Mapstone

✓ This study was undertaken to evaluate the role of two sets of growth factors, platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-β), in the induction and maintenance of glial tumors and their phenotypic expression. Explants from eight malignant tumors, five benign tumors, and two nontumor glial cells were analyzed for levels of messenger ribonucleic acid (mRNA) expression of PDGFA, PDGFB, TGF-β1, and TGF-β2. Results were normalized to the mRNA expression of tubulin, a “housekeeping” gene present in glial cells. Of the 15 explants tested, PDGFB was seen in six, all of which were malignant tumors; PDGFA was seen in all 15 with much higher levels expressed in malignant tumors; and TGF-β1 and TGF-β2 were seen in all 15 without a clear difference between cell types, although expression tended to be higher in malignant tumors. This project supports the theory that the induction and maintenance of glial tumors is likely to be a multifactorial phenomenon.


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