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Expression data from laser microdissected murine intestinal epithelial cells

ABSTRACT: Microarray analyses of laser microdissected murine intestinal epithelial cells under the control of maternal inflammation at 17.5 days post conception demonstrates that maternal inflammation differentially regulates 2174 (iWT) and 3345 (iARE) genes in fetal tissue, but these transcriptional profiles were overwritten in the postnatal environment dominated by tissue inflammation at 8 weeks postnatal. We isolated 50 ng total RNA out of laser microdissected fetal and adult intestinal epithelial cells from the distal ileum and performed microarrays to address whether maternal inflammation programs the fetal intestine towards TNF-driven pathology Conventionally raised heterozygous TnfM-NM-^TARE/+ and Tnf+/+ wild type mice on C57BL/6 background were used for this study. Female Tnf+/+ wild type (WT) mice were bred with male TnfM-NM-^TARE/+ (ARE) mice and vice versa, generating offspring from healthy WT dams (WT and ARE) and inflamed ARE dams (iWT and iARE). On day 17.5 post conception (dpc) and 8 weeks postnatal the fetuses and offspring were sacrificed.The gut was freshly frozen in Optimal Cutting Temperature (O.C.T.) embedding compound (Sakura Finetek, Torrance, USA) on dry ice and stored at -80M-BM-0C until laser microdissection.

ORGANISM(S): Mus musculus

SUBMITTER: Jana Hemmerling

PROVIDER: E-GEOD-44433 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from laser microdissected murine intestinal epithelial cells

Project description:Microarray analyses of laser microdissected murine intestinal epithelial cells under the control of maternal inflammation at 17.5 days post conception demonstrates that maternal inflammation differentially regulates 2174 (iWT) and 3345 (iARE) genes in fetal tissue, but these transcriptional profiles were overwritten in the postnatal environment dominated by tissue inflammation at 8 weeks postnatal. We isolated 50 ng total RNA out of laser microdissected fetal and adult intestinal epithelial cells from the distal ileum and performed microarrays to address whether maternal inflammation programs the fetal intestine towards TNF-driven pathology

2014-05-05 | GSE44433 | GEO

ASA404 and TNFM-NM-1 treatment in preclinical models of endocrine tumors is associated with differential TNF-R 1 and TLR- 4 M-bM-^@M-^Ssignaling

Project description:Purpose: ASA404 (Vadimezan) belongs to a class of agents with disrupting properties against tumor vasculature, which is partly mediated by TNFM-NM-1-signaling. Our aim was to investigate the potential therapeutic applicability of ASA404 against endocrine tumors. Experimental Design: We determined anti-tumoral effects in preclinical models of neuroendocrine tumors of the gastroenteropancreatic system [1] and adrenocortical cancer (NCI-H295R) by histology and immunohistochemistry. Furthermore, we characterized these models with their clearly different responsiveness regarding TNFM-NM-1 synthesis and signaling. Results: Upon treatment of tumor bearing mice significant anti-tumoral effects, an increase in TNFM-NM-1 as well as TNFM-NM-1-specific activation of downstream signaling were evident in the BON tumor model while no comparable effects were detectable for NCI-H295R. Two important modulator of TNFM-NM-1-signaling, toll-like-receptor 4 (TLR-4) and its adaptor protein LY96 were found highly expressed in BON tumors and transgenic expression in NCI-H295R partly restored TNFM-NM-1 responsiveness. Furthermore, expression of IRAK2-kinase, which has recently been linked to TLR-4-signaling as a mediator of sustained TNFM-NM-1 release was induced upon TNFM-NM-1-treatment in BON, but not in NCI-H295R cells. Finally, we identified TNFAIP3/A20, a member of an inhibitory feedback-loop downstream of both investigated signaling cascades, as overexpressed in the adrenocortical carcinoma tumor model. Subsequent analyses of clinical patient samples confirmed a correlation between tumor TNFAIP3 expression levels and overall survival in patients with ACC. Conclusions: Taken together our findings provide evidence that modulation of TNFM-NM-1-signaling could be of relevance both for the clinical course of ACC patients and as a marker of treatment response. BON or NCI-H295R tumor cells were treated in-vitro with TNFalpha and compared to unstimulated cells

2014-12-17 | E-GEOD-64250 | biostudies-arrayexpress

Impact of Maternal Immune Activation and Sex on Placental and Fetal Brain Cytokine and Gene Expression Profiles in a Preclinical Model of Neurodevelopmental Disorders

Project description:Maternal inflammation during gestation is associated with a later diagnosis of neurodevelopmental disorders including autism spectrum disorder (ASD). However, the specific impact of maternal immune activation (MIA) on placental and fetal brain development remains insufficiently understood. This study aimed to investigate the effects of MIA by analyzing placental and brain tissues obtained from the offspring of pregnant dams exposed to polyinosinic:polycytidylic acid (Poly I:C) on embryonic day 12.5. Cytokine and mRNA content in the placenta and brain tissues were assessed using multiplex cytokine assays and bulk-RNA sequencing on embryonic day 17.5. Bulk-RNA sequencing was performed on placenta and brain tissues on embryonic day 17.5.

2024-05-15 | GSE248222 | GEO

Maternal hematopoietic TNF, via milk chemokines, programs hippocampal development and memory

Project description:TNF is a proinflammatory cytokine with established roles in host defense and immune system organogenesis. Here we report a novel physiological function of TNF that extends its effect beyond the host into the developing offspring. A partial/complete maternal TNF-deficit, specifically in hematopoietic cells, resulted in reduced milk levels of chemokines IP-10, MCP-1/-3/-5, and MIP-1β, which in turn, augmented offspring postnatal hippocampal proliferation, leading to improved adult spatial memory. These effects were reproduced by the postpartum administration of a clinically used anti-TNF agent. Chemokines, fed to suckling pups of TNF-deficient mothers, restored both postnatal proliferation and adult spatial memory to normal levels. This work identifies a TNF-dependent “lactrocrine” pathway that programs offspring hippocampal development and memory. The level of ambient TNF is known to be downregulated by physical activity/exercise and adaptive stress; thus, we propose that the maternal TNF-milk chemokine pathway evolved to promote offspring adaptation to post-weaning environmental challenges/competition. Examined transcriptomes of TNF wild type offspring of TNF wild type or heterozygouse mothers

2013-12-01 | E-GEOD-52069 | biostudies-arrayexpress

Maternal hematopoietic TNF, via milk chemokines, programs hippocampal development and memory

2013-12-01 | GSE52069 | GEO

Thyroid Hormone Action Controls Multiple Components of Cell Junctions at the Ventricular Zone in the Newborn Rat Brain

Project description:We investigated if developmental hypothyroidism controlled cell signaling in the ventricular zone of the rat brain on postnatal day 2. We performed laser capture microdissection to isolate the ventricular zone in euthyroid (control) and hypothyroid rats. Hypothyroidism was induced by a maternal exposure to the goitrogen propylthiourail (PTU) during pregnancy and lactation.

2023-01-23 | GSE218930 | GEO

Maternal western diet primes susceptibility to hepatic inflamation in adult male mouse offspring

Project description:Background & Aims: The influences of the maternal diet during gestation has been suggested to be involved in the development of different aspects of the metabolic syndrome. In our mouse model we characterised the role of maternal western diet in the development of non-alcoholic fatty liver disease (NAFLD) in the offspring. Methods: Female mice were fed either a western (W) or low-fat control (L) semi-synthetic diet before and during gestation and lactation. At weaning, male offspring were assigned either the W or the L diet, generating four experimental groups: WW, WL, LW and LL offspring. Biochemical, histological and epigenetic indicators were investigated at 29 weeks of age. Results: Male offspring exposed to prenatal western style diet and to a post-weaning W diet (WW) showed hepatomegaly combined with increased hepatic cholesterol and triglycerides accumulation, compared to LW offspring. This was associated with up-regulation of de novo lipid synthesis and dysregulation of beta oxidation and lipid storage. Elevated hepatic transaminases and increased expression of Tnfa, Cd11, Mcp1 and Tgfb underpin the severity of liver injury. Histological analysis supported the presence of steatohepatitis in the WW offspring. In addition alterations in DNA methylation in key metabolic genes (Ppara, Insig, Fasn) were detected. Conclusion: Maternal dietary fat intake during critical developmental phases programs susceptibility to liver disease in mouse offspring. This was mediated by shifts in lipid metabolism and inflammatory response. Long lasting epigenetic changes may underlie this dysregulation 4 groups of 6 male mouse were analysed , 1 experimental and 1 biological outlier was excluded , so n=6,5,5,6 in the 4 groups (LL,LW,WL,WW)

2014-01-21 | E-GEOD-44901 | biostudies-arrayexpress

Early growth response protein-1 coordinates lipotoxicity-associated placental inflammation: Role in Maternal Obesity

Project description:Maternal obesity during pregnancy leads to a pro-inflammatory milieu in the placenta. We conducted a global transcriptomic profiling in BeWo cells following palmitic acid (PA, 500 uM) and/or TNF-alpha (10 ng/ml) treatment for 24 h. Microarray analysis revealed that placental cytotrophoblasts increased expression of genes related to inflammation, stress response and immediate-early factors in response to plamitic acid, TNF-alpha or a combination of both. Our results suggest that fatty acids and inflammatory cytokines induce inflammation in placental cells via activation of JNK-Egr-1 signaling. global transcriptomic profiling in BeWo cells following palmitic acid (PA, 500 uM) and/or TNF-alpha (10 ng/ml) treatment for 24 h

2014-01-21 | E-GEOD-43685 | biostudies-arrayexpress

Genome-wide TNFM-NM-1-induced p65 binding before and after telomerase inhibition in HeLa cells

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) was performed to analyze the effect of telomerase inhibition on TNFM-NM-1-induced genome-wide p65 binding in HeLa cells. By obtaining over 40 million uniquely mappable reads per sample from ChIP-seq, maps for TNFM-NM-1-induced p65 binding in absence and presence of an hTERT inhibitor, MST-312, were generated. As expected, TNFM-NM-1 treatment significantly increased genome-wide p65 occupancy. Interestingly, when cells were treated with MST-312 prior to TNFM-NM-1 stimulation, the number of p65 binding sites was reduced. In addition, some binding sites, including important p65 targets like IL6 and TNF, showed a reduced p65 occupancy with a minimum fold change of 1.5, after MST-312 exposure. Taken together, our ChIP-seq data indicate that telomerase is required for optimal p65 binding at a small proportion of p65 target sites upon inflammatory stimuli. Examination of p65 binding in HeLa cells in absence and presence of TNFM-NM-1 and MST-312.

2012-11-26 | E-GEOD-41100 | biostudies-arrayexpress

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