Effect of litter birth weight phenotype on transcriptomic response to swine influenza virus infection in pig lung
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ABSTRACT:
ORGANISM(S): Sus scrofa
PROVIDER: GSE62765 | GEO | 2015/10/27
SECONDARY ACCESSION(S): PRJNA265090
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of gene expression in the lungs of pigs from high and low litter birth weight groups (HBW and LBW) inoculated with swine influenza virus. The aim of the experiment is to determine whether litter birth weight has an effect on the innate immune response to infection in pigs, and whether differences in gene expression can be linked to epigenetic differences between the two birth weight groups. A two condition experiment: lung tissue RNA from HBW and LBW SIV-infected pigs. 16 biological replicates for each condition, each hybridized with a reference to separate arrays. 32 arrays in total.
2015-10-27 | E-GEOD-62765 | biostudies-arrayexpress
Project description:Comparison of gene expression in the lungs of pigs classified as Resistant (RES) or Susceptible (SUS) to influenza pathology based on clinical lesion scores. The aim of the experiment is to identify genes whose expression is associated with resistance/susceptibility to influenza pathology. These are a subset of animals selected from a larger experiment that investigated the effect of low (LBW) or high (HBW) litter birth weight phenotype on influenza pathology.
2015-10-27 | GSE62768 | GEO
Project description:Low Birth Weight (LBW) newborns (with weight less than 2500g) suffer a higher frequency and severity of microbial infection than normal birth weight (NBW) newborns. Morbidity and mortality of LBW infants due to infectious diseases are known to be high and it has been associated with compromised immune functions, however, the complete understanding of the cause is lacking. We, therefore, conducted a gene expression study to identify all the defective pathways and functions in the LBW newborns using DNA microarray. RNA were isolated from the umbilical cord blood of the NBW and LBW newborns and processed for chip hybridisation. Our results suggest down-regulation of genes participating in several canonical pathways vital in the defense response against microbes and perpetuation of immune responses. Pattern recognition receptors (PRRs) and Interferon signaling appear to be most significantly impacted pathways. The information generated from this study may help in depth understanding of the cause of higher frequency of infections in LBW and thus, in turn help devise better therapeutic interventions.
2012-01-15 | GSE29807 | GEO
Project description:Low Birth Weight (LBW) newborns (with weight less than 2500g) suffer a higher frequency and severity of microbial infection than normal birth weight (NBW) newborns. Morbidity and mortality of LBW infants due to infectious diseases are known to be high and it has been associated with compromised immune functions, however, the complete understanding of the cause is lacking. We, therefore, conducted a gene expression study to identify all the defective pathways and functions in the LBW newborns using DNA microarray. RNA were isolated from the umbilical cord blood of the NBW and LBW newborns and processed for chip hybridisation. Our results suggest down-regulation of genes participating in several canonical pathways vital in the defense response against microbes and perpetuation of immune responses. Pattern recognition receptors (PRRs) and Interferon signaling appear to be most significantly impacted pathways. The information generated from this study may help in depth understanding of the cause of higher frequency of infections in LBW and thus, in turn help devise better therapeutic interventions. Total 12 subjects were included in the study. 4 NBW newborns umblical cord blood samples served as control and 8 LBW newborns umblical cord blood samples were treated as the experimental samples for the study.
2012-01-15 | E-GEOD-29807 | biostudies-arrayexpress
Project description:We aimed to gain mechanistic insights into the impact of uteroplacental insufficiency upon hepatic cholestrol metabolism pathways in young adult offspring.Uterine artery ablation-induced low birth weight (LBW) and normal birth weight (NBW) male and female guinea pig offspring were fed a control diet from weaning until postnatal day 150. Analysis of whole hepatic transcriptome results identified that between LBW and NBW offspring livers, 51 (29 up-regulated and 22 down-regulated) and 31 (8 up-regulated and 23 down-regulated) genes were differentially expressed in males and females respectively (fold change| >= 2 and p-value < 0.05). KEGG pathway analysis of these differentially expressed genes revealed that “Cholesterol metabolism” was an enriched pathway in LBW males but not females (p<0.05).
2020-11-10 | GSE161124 | GEO
Project description:We investigated the molecular pathogenesis of LBW rats obtained by intraperitoneal injection of dexamethasone into pregnant animals. Normal-birth-weight (NBW) rats were used as controls with seven animals per group. When the rats were four weeks old, the left kidneys were removed and used for comprehensive label-free proteomic studies
2022-02-15 | PXD018948 | Pride
Project description:OBJECTIVE: To characterize the hormonal milieu and adipose gene expression in response to catch-up growth (CUG), a growth pattern associated with obesity and diabetes risk, in a mouse model of low birth weight (LBW). RESEARCH DESIGN AND METHODS: ICR mice were food restricted by 50% from gestational days 12.5-18.5, reducing offspring birth weight by 25%. During the suckling period, dams were either fed ad libitum, permitting CUG in offspring, or food restricted, preventing CUG. Offspring were killed at age 3 weeks, and gonadal fat was removed for RNA extraction, array analysis, RT-PCR, and evaluation of cell size and number. Serum insulin, thyroxine (T4), corticosterone, and adipokines were measured. RESULTS: At age 3 weeks, LBW mice with CUG (designated U-C) had body weight comparable with controls (designated C-C); weight was reduced by 49% in LBW mice without CUG (designated U-U). Adiposity was altered by postnatal nutrition, with gonadal fat increased by 50% in U-C and decreased by 58% in U-U mice (P < 0.05 vs. C-C mice). Adipose expression of the lipogenic genes Fasn, AccI, Lpin1, and Srebf1 was significantly increased in U-C compared with both C-C and U-U mice (P < 0.05). Mitochondrial DNA copy number was reduced by >50% in U-C versus U-U mice (P = 0.014). Although cell numbers did not differ, mean adipocyte diameter was increased in U-C and reduced in U-U mice (P < 0.01). CONCLUSIONS: CUG results in increased adipose tissue lipogenic gene expression and adipocyte diameter but not increased cellularity, suggesting that catch-up fat is primarily associated with lipogenesis rather than adipogenesis in this murine model. Epididymal fat samples were obtained at age 3 weeks from 5 control mice (CC), 5 mice exposed to in utero undernutrition (UC), and 4 mice exposed to undernutrition in utero and during suckling (UU).
2010-03-04 | E-GEOD-16083 | biostudies-arrayexpress
Project description:OBJECTIVE: To characterize the hormonal milieu and adipose gene expression in response to catch-up growth (CUG), a growth pattern associated with obesity and diabetes risk, in a mouse model of low birth weight (LBW). RESEARCH DESIGN AND METHODS: ICR mice were food restricted by 50% from gestational days 12.5-18.5, reducing offspring birth weight by 25%. During the suckling period, dams were either fed ad libitum, permitting CUG in offspring, or food restricted, preventing CUG. Offspring were killed at age 3 weeks, and gonadal fat was removed for RNA extraction, array analysis, RT-PCR, and evaluation of cell size and number. Serum insulin, thyroxine (T4), corticosterone, and adipokines were measured. RESULTS: At age 3 weeks, LBW mice with CUG (designated U-C) had body weight comparable with controls (designated C-C); weight was reduced by 49% in LBW mice without CUG (designated U-U). Adiposity was altered by postnatal nutrition, with gonadal fat increased by 50% in U-C and decreased by 58% in U-U mice (P < 0.05 vs. C-C mice). Adipose expression of the lipogenic genes Fasn, AccI, Lpin1, and Srebf1 was significantly increased in U-C compared with both C-C and U-U mice (P < 0.05). Mitochondrial DNA copy number was reduced by >50% in U-C versus U-U mice (P = 0.014). Although cell numbers did not differ, mean adipocyte diameter was increased in U-C and reduced in U-U mice (P < 0.01). CONCLUSIONS: CUG results in increased adipose tissue lipogenic gene expression and adipocyte diameter but not increased cellularity, suggesting that catch-up fat is primarily associated with lipogenesis rather than adipogenesis in this murine model.
2009-05-14 | GSE16083 | GEO
Project description:Sub-optimal fetal development is associated with an increased risk of developing cardiovascular disease, type 2 diabetes (T2D) and adiposity later in life. However, definitions of intrauterine growth restriction (IUGR) and small for gestational age (SGA) are based on simple statistical approaches that may misclassify infants with a normal developmental profile and vice versa. We used an unbiased global profiling approach to identify gene expression patterns in umbilical cord tissue from 38 infants and identified a set of 466 genes which separated the subjects into 2 distinct groups – one biased towards lower birth weight and one biased towards normal birth weight. The data suggest that approximately 30% of children of normal size have a molecular profile more typical of impaired fetal development and who may be on a programmed trajectory. Differences in expression between the two groups encompassed 384 upregulated and 82 downregulated genes. Molecular profiling at birth may have utility in identifying markers that potentially reflect antenatal developmental and may be predictive of future phenotypic development after birth. Importantly, it may provide an alternative to the current classification of infants using birth weights. RNA from umbilical cord tissue from full term neonates was extracted and hybridized. Separation into 2 distinct groups, independent of birth weight, but based solely on gene expression levels was analysed by Genespring. After appropriate statistical analysis, one group was keenly associated with a higher birth weight (22 samples) while the other was associated with a lower birth-weight (18 samples). Technical replicates were included for all 40 samples.
2011-10-20 | E-GEOD-24818 | biostudies-arrayexpress
Project description:Sub-optimal fetal development is associated with an increased risk of developing cardiovascular disease, type 2 diabetes (T2D) and adiposity later in life. However, definitions of intrauterine growth restriction (IUGR) and small for gestational age (SGA) are based on simple statistical approaches that may misclassify infants with a normal developmental profile and vice versa. We used an unbiased global profiling approach to identify gene expression patterns in umbilical cord tissue from 38 infants and identified a set of 466 genes which separated the subjects into 2 distinct groups – one biased towards lower birth weight and one biased towards normal birth weight. The data suggest that approximately 30% of children of normal size have a molecular profile more typical of impaired fetal development and who may be on a programmed trajectory. Differences in expression between the two groups encompassed 384 upregulated and 82 downregulated genes. Molecular profiling at birth may have utility in identifying markers that potentially reflect antenatal developmental and may be predictive of future phenotypic development after birth. Importantly, it may provide an alternative to the current classification of infants using birth weights.
2011-10-21 | GSE24818 | GEO