Gene expression in adipose tissue of intrauterine growth restricted (IUGR) and Macrosomic animals that developed in a crowded uterine horn
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE33761 | GEO | 2012/04/25
SECONDARY ACCESSION(S): PRJNA148391
REPOSITORIES: GEO
Similar Datasets
Project description:Animals that are growth restricted in utero may show rapid postnatal growth that ultimately results in adult obesity. Macrosomic animals at birth typically remain large and are also obese as adults. Our goal was to examine the differences between animals that reach obesity in different ways. We also aimed to examine gene expression in animals that start out lean and stay lean compared to those that start out lean and become fat. We used microarrays to detail gene expression in adipose tissue. 3 samples each from IUGR animals with rapid postnatal growth (IH), IUGR animals with slower postnatal growth (IL), and macromsomic animals (M).
2012-04-24 | E-GEOD-33761 | biostudies-arrayexpress
Project description:Intrauterine growth restriction (IUGR) is a serious pathological complication associated with compromised fetal development during pregnancy. The aim of the study was to broaden knowledge about the transcriptomic complexity of the human placenta by identifying genes potentially involved in IUGR pathophysiology. RNA-Seq data were used to profile protein-coding genes, detect alternative splicing events (AS), single nucleotide variant (SNV) calling, and RNA editing sites prediction in IUGR-affected placental transcriptome. The applied methodology enabled detection of 37,501 transcriptionally active regions and the selection of 28 differentially-expressed genes (DEGs), among them 10 were upregulated and 18 downregulated in IUGR-affected placentas. Functional enrichment annotation indicated that most of the DEGs were implicated in the processes of inflammation and immune disorders related to IUGR and preeclampsia. Additionally, we revealed that some genes (S100A13, GPR126, CTRP1, and TFPI) involved in the alternation of splicing events were mainly implicated in angiogenic-related processes. Significant SNVs were overlapped with 6533 transcripts and assigned to 2386 coding sequence (CDS), 1528 introns, 345 5' untranslated region (UTR), 1260 3'UTR, 918 non-coding RNA (ncRNA), and 10 intergenic regions. Within CDS regions, 543 missense substitutions with functional effects were recognized. Two known mutations (rs4575, synonymous; rs3817, on the downstream region) were detected within the range of AS and DEG candidates: PA28β and PINLYP, respectively. Novel genes that are dysregulated in IUGR were detected in the current research. Investigating genes underlying the IUGR is crucial for identification of mechanisms regulating placental development during a complicated pregnancy.
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Project description:BACKGROUND:To explore the hypothesis that maternal periodontitis is associated with increased risk for Intrauterine Growth Restriction (IUGR), we examined the risk of IUGR in relation to periodontal treatment before, during and after pregnancy. METHODS:We conducted a retrospective cohort analysis of insurance claims data from 2009 to 2012 for women who delivered a singleton live birth (n?=?32,168). IUGR was examined as a function of type and timing of dental treatment, adjusting for potential confounders in logistic regression. Sensitivity analysis evaluated the potential effects of unmeasured confounding. RESULTS:Women who received periodontal treatment after delivery, indicating the presence of untreated periodontal disease during pregnancy, had significantly higher odds of IUGR compared to women who received no periodontal treatment (adjusted OR 1.5, 95% CI 1.2, 1.8). CONCLUSIONS:Periodontal treatment provided in the immediate postpartum period, a proxy for periodontitis during gestation, was associated with increased risk of IUGR.
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Project description:Dishevelled family proteins (DVL1, DVL2, and DVL3) are cytoplasmic proteins that are involved in canonical and non-canonical Wnt signaling pathway during embryonic development. The role of DVL proteins in the placental tissue remains mostly unknown. In the current study, we explored the role of Dishevelled proteins in naturally invasive tissue, trophoblast. Formalin-fixed paraffin-embedded samples of 15 term placentas from physiologic term pregnancies and 15 term placentas from pregnancies complicated with intrauterine growth restrictions (IUGR) were used for the study. Expression levels of mRNA for DVL1, DVL2, and DVL3 in placentas were analyzed by quantitative real-time PCR (qRTPCR). DVL1, DVL2, and DVL3 protein expression were semi-quantitatively analyzed using immunohistochemistry. The expression of DVL2 and DVL3 proteins was significantly higher in trophoblasts in placental villi from IUGR pregnancies compared with the control group of term placentas. In contrast, DVL3 protein expression was significantly higher in endothelial cells in placental villi from IUGR pregnancies compared with normal term placentas. The observed differences at protein levels between normal and IUGR placentas were not confirmed at the mRNA levels of DVL genes. Our data indicate the active involvement of DVL proteins in IUGR-related placentas. No significant changes were observed in DVL mRNA levels between the two groups of placentas. Further studies are required to explore the clinical relevance of these observations.
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Project description:Epithelial cells provide an initial line of defense against damage and pathogens in barrier tissues such as the skin; however this balance is disrupted in obesity and metabolic disease. Skin gamma delta T cells recognize epithelial damage and release cytokines and growth factors that facilitate wound repair. To determine the impact of obesity and metabolic disease on skin gamma delta T cells, we isolated skin gamma delta T cells from 10-week old C57BLKS/J lean db/+ and obese db/db animals for further study. Due to a deficiency in the leptin receptor (db), homozygous db/db animals do not process satiety signals, continually eat and develop severe obesity and metabolic disease. Skin gamma delta T cells isolated from these animals were compared for changes in mRNA expression using microarray. We have determined that obesity and metabolic disease negatively impacts homeostasis and functionality of skin gamma delta T cells, rendering host defense mechanisms vulnerable to injury and infection. The goal of this experiment was to compare skin gamma delta T cells in a control mouse to skin gamma delta T cells isolated from an obese mouse to see what homeostatic changes occur in obesity and metabolic disease. gamma delta T cells were isolated from two 10-week old lean db/+ control and two 10-week old obese db/db animals for comparison. We wanted to determine which growth factors and signaling pathways were altered in skin gamma delta T cells residing in the obese environment.
2010-07-30 | E-GEOD-22196 | biostudies-arrayexpress
Project description:From a forward mutagenetic screen to discover mutations associated with obesity, we identified mutations in the spag7 gene linked to metabolic dysfunction in mice. Here we show that SPAG7 KO mice are born smaller and develop obesity and glucose intolerance in adulthood. This obesity does not stem from hyperphagia, but a decrease in energy expenditure. The KO animals also display reduced exercise tolerance and muscle function due to impaired mitochondrial function. Furthermore, SPAG7-deficiency in developing embryos leads to intrauterine growth restriction, brought on by placental insufficiency, likely due to abnormal development of the placental junctional zone. This insufficiency leads to loss of SPAG7-deficient fetuses in utero and reduced birth weights of those that survive. We hypothesize that a “thrifty phenotype” is ingrained in SPAG7 KO animals during development that leads to adult obesity. Collectively, these results indicate that SPAG7 is essential for embryonic development and energy homeostasis later in life.
2023-11-01 | GSE246428 | GEO
Project description:In this study, our aims were to characterize oligodendrogenesis alterations in fetuses with intrauterine growth restriction (IUGR) and to find therapeutic strategies to prevent/treat them using a novel rabbit in vitro neurosphere culture. IUGR was surgically induced in one uterine horn of pregnant rabbits, while the contralateral horn served as a control. Neural progenitor cells (NPCs) were obtained from pup's whole brain and cultured as neurospheres mimicking the basic processes of brain development including migration and cell differentiation. Five substances, chosen based on evidence provided in the literature, were screened in vitro in neurospheres from untreated rabbits: Docosahexaenoic acid (DHA), melatonin (MEL), zinc, 3,3',5-Triiodo-L-thyronine (T3), and lactoferrin (LF) or its metabolite sialic acid (SA). DHA, MEL and LF were further selected for in vivo administration and subsequent evaluation in the Neurosphere Assay. In the IUGR culture, we observed a significantly reduced percentage of oligodendrocytes (OLs) which correlated with clinical findings indicating white matter injury in IUGR infants. We identified DHA and MEL as the most effective therapies. In all cases, our in vitro rabbit neurosphere assay predicted the outcome of the in vivo administration of the therapies and confirmed the reliability of the model, making it a powerful and consistent tool to select new neuroprotective therapies.
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Project description:Immunotherapy is life saving for some cancer patients and while obesity can promote cancer, it may also increase immunotherapy efficacy. Mechanisms of this effect have been unclear, although obesity can promote an inflammatory state that may modify tumor infiltrating lymphocytes and tumor associated macrophage (TAM) populations in tumors. To identify mechanisms by which obesity affects anti-tumor immunity, diet-induced obese and lean C57BL/6 mice received subcutaneous murine MC38-CEA1 colon cancer tumors. Obesity increased tumor growth rate and tumor burden. Fewer immune cells were present in tumors from obese mice, and the T cells had an activated and exhausted phenotype. Macrophages in obese animals had decreased expression of iNOS2 and MHCII, supporting a weaker “M1” anti-tumor phenotype compared to lean mice. When treated with anti-PD-1 antibodies, however, obese mice had a greater absolute decrease in tumor burden than lean mice. PD-1 blockade repolarized the macrophages to an M1-phentoype in obese mice, but this did not occur in the lean mice. Mechanistically, leptin is a pro-inflammatory adipokine that is increased in obesity and may mediate enhanced anti-tumor immunity in obesity. To test the effect of leptin on tumor growth and anti-tumor immunity, lean mice were treated with leptin and tumors were observed over time. Leptin had single-agent preventative and therapeutic anti-tumor efficacy similar to PD-1 checkpoint therapy. These data demonstrate that obesity has dual effects in cancer through promotion of tumor cell initiation while also enhancing anti-tumor immunity through elevated levels of leptin that can reprogram inflammatory macrophages.
2021-10-06 | GSE179936 | GEO
Project description:Obesity is a heterogeneous conditions comprising obese individuals with metabolic disorders (termed metabolically unhealthy obese; MUO) and obese individuals who are metabolically healthy (termed metabolically healthy obese; MHO). We used microarrays to examine differences in subcutaneous adipose tissue gene expression from lean healthy (LH), metabolically healthy obese (MHO), and metabolically unhealthy obese (MUO) individuals.
2014-11-14 | GSE55200 | GEO
Project description:Obesity and physical inactivity have a profound impact on skeletal muscle metabolism. In the present work, we have investigated differences in protein expression and energy metabolism in primary human skeletal muscle cells established from lean donors (BMI<25 kg/m2) and individuals with obesity (BMI>30 kg/m2). Furthermore, we have studied the effect of fatty acid pretreatment on energy metabolism in myotubes from these donor groups. Alterations in protein expression were investigated using proteomic analysis, and energy metabolism was studied using radiolabeled substrates. Gene Ontology enrichment analysis showed that glycolytic, apoptotic, and hypoxia pathways were upregulated, whereas the pentose phosphate pathway was downregulated in myotubes from donors with obesity compared to myotubes from lean donors. Moreover, fatty acid, glucose, and amino acid uptake were increased in myotubes from individuals with obesity. However, fatty acid oxidation was reduced, glucose oxidation was increased in myotubes from subjects with obesity compared to cells from lean. Pretreatment of myotubes with palmitic acid (PA) or eicosapentaenoic acid (EPA) for 24 h increased glucose oxidation and oleic acid uptake. EPA pretreatment increased the glucose and fatty acid uptake and reduced leucine fractional oxidation in myotubes from donors with obesity. In conclusion, these results suggest that myotubes from individuals with obesity showed increased fatty acid, glucose, and amino acid uptake compared to cells from lean donors. Furthermore, myotubes from individuals with obesity had reduced fatty acid oxidative capacity, increased glucose oxidation, and a higher glycolytic reserve capacity compared to cells from lean donors. Fatty acid pretreatment enhances glucose metabolism, and EPA reduces oleic acid and leucine fractional oxidation in myotubes from donor with obesity, suggesting increased metabolic flexibility after EPA treatment
2023-03-11 | PXD037909 | Pride