Chronic oral administration of nicotine affects transcriptomic profiling in conditional Presenilin 1/2 knockout mice and wild type mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE211983 | GEO | 2024/01/01
REPOSITORIES: GEO
Similar Datasets
Project description:Inflammation and elastin degradation are key hallmarks in the pathogenesis of abdominal aortic aneurysms (AAA). It has been acknowledged that activation of alpha7 nicotinic acetylcholine receptors (α7nAChRs) attenuates inflammation, termed the cholinergic anti-inflammatory pathway (CAP). Thus, we hypothesized that low-dose nicotine, an α7nAChR agonist, impairs the progression of AAAs in rats by activating the CAP. Male Sprague-Dawley rats underwent surgical AAA induction with intraluminal elastase infusion. We compared vehicle rats with rats treated with nicotine (1.25 mg/kg/day) and the aneurysm progression was monitored by weekly ultrasound images for 28 days. Nicotine significantly promoted AAA progression after 28 days of treatment (p=0.031). Additionally, gelatin zymography demonstrated that nicotine significantly reduced pro-matrix metalloprotease (pro-MMP) 2(p=0.029) and MMP9(p=0.030) activity in aneurysmal tissue. No significant difference was found in elastin content or the score of elastin degradation between the groups. Neither infiltrating neutrophils nor macrophages, nor aneurysmal messenger RNA (mRNA) levels of pro- or anti-inflammatory cytokines differed between the vehicle and nicotine group. Finally, no difference in mRNA levels of markers for antioxidative stress or vascular smooth muscle cells contractile phenotype was observed. However, proteomics analyses of non-aneurysmal abdominal aortas revealed that nicotine decreased proteins in the ontology terms inflammation and reactive oxygen species and in contradiction to augmented AAAs. In conclusion, treatment with the given nicotine dose augmented AAA progression in this rat model.
2023-07-20 | PXD040414 | Pride
Project description:Gene expression profile of presenilin conditional double knockout cerebral cortex, comparing to control. Age of mice: 6 months
2008-06-11 | E-GEOD-1375 | biostudies-arrayexpress
Project description:We have performed gene expression microarry analysis to profile molecular alterations in normal human oral keratinocytes that are induced by EtOH and/or nicotine. Our goal is to examine molecular signatures that are dysregulated by EtOH or nicotine and define the effects of co-use of alcohol and nicotine on normal oral epithelial cells and potentially on carcinogenesis.
2014-05-14 | GSE57634 | GEO
Project description:We have performed gene expression microarry analysis to profile molecular alterations in normal human oral keratinocytes that are induced by EtOH and/or nicotine. Our goal is to examine molecular signatures that are dysregulated by EtOH or nicotine and define the effects of co-use of alcohol and nicotine on normal oral epithelial cells and potentially on carcinogenesis. Primary normal human oral keratinocytes were cultured and treated with various dose of EtOH (0, 20 and 50 mM) and cotreated with various dose of nicotine (0, 0.5 and 1uM) for 24 hours. Total RNA was isolated and subjected to gene expression microarray analysis using Affymetrix Human Genome 2.0 plus.
2014-05-14 | E-GEOD-57634 | biostudies-arrayexpress
Project description:We tested the effects of chronic paternal nicotine exposure in C57BL6/J mice on hippocampal DNA methylation in F1 offspring.
2019-11-25 | GSE140904 | GEO
Project description:We tested the effects of chronic paternal nicotine exposure in C57BL6/J mice on hippocampal RNA expression in F1 offspring.
2019-11-25 | GSE140903 | GEO
Project description:Our laboratory previous research confirmed that nicotine in cigarette smoke causes apoptosis in germ cells in the testis and it will increase the formation of autophagosomes in the cytoplasm of testicular stromal cells. In addition, nicotine, the main toxic substance in cigarette smoke, also affects telomerase activity of spermatogenic cells, shortens telomere length, and causes structural damage of chromosomes. It is worth noting that after nicotine treatment, the expression of proteins involved in cytoskeleton regulation and energy metabolism in mouse testis was significantly up-regulated, and the sperm motility of mice was improved after nicotine treatment. To investigate the underlying mechanism, C57BL/6J mice were divided into control and nicotine treated groups. Next generation RNA sequencing and bio-informatics analysis were carried out to analysis the effects of nicotine on the RNA profile of mice spermatozoa. The results of RNA-Seq showed that the number of reads in the control group was 2089729, and the number of reads in the nicotine-treated group was 1739093, and a total of 8699 transcripts were obtained. Expression level of some pathways remarkably changed after nicotine treatment.This experimental study are helpful to understand the mechanism of the effect of nicotine on sperm and help us to provide a way to study the effection of patern nicotine exposure on offspring development.
2021-07-31 | GSE155145 | GEO
Project description:Regulation of presenilin genes. Presenilins are intramembrane aspartic proteases. These proteases are critical proteins in pathogenesis of Alzheimer's disease. The function of recently identified presenilin-homologous proteases (IMPAS or SPP)s is unknown. Our preliminary data in C.elegans model suggested the role of these proteins in early-development and , perhaps, in pathway related- to cholesterol -regulated signalling (Grigorenko et al, 2004, PNAS). The overall goal is to determine pattern of gene expression alterations in cells with knock-out or knock-down presenilin related proteins (IMPAS). The cultured cells, C.elegans and mouse models are planned to be used in this study. Here , we will determine gene expression patterns in C.elegans strain NL2099, fed with bacteria HT115, producing dsRNA for Ce-imp-2 gene (knock-down of imp-2 gene by RNAi )or GFP gene as a control. We hypothesize that novel family of presenilin-related proteases is important for cholesterol-regulated intracellular signalling and early development (including CNS/neuronal development and function). C.elegans (strain NL2099) on L1 stage were placed on agarose plates with bacteria HT115, producing dsRNA for: 1) Ce-imp-2 gene; 2) GFP as a control gene. After 48 hours at 20C , worms were washed in M9 buffer and total RNA was isolated by TRIzol method.
2008-06-15 | E-GEOD-7354 | biostudies-arrayexpress
Project description:Notch1 signaling is an important regulator of cell fate in early stages of T cell development. Because Notch receptors can function redundantly, we sought an approach for inhibiting all endogenous Notch signaling in thymocytes. Upon ligand engagement, Notch receptors undergo two successive proteolytic cleavages, the second involving a Presenilin (PS) containing complex with -secretase activity that releases a small intracellular fragment of Notch. This activated form of Notch (NotchIC) translocates from the membrane to the nucleus, where it acts as a transcription factor, inducing the expression of multiple target genes . Since Presenilins are required for the activation of all four mammalian forms of Notch, we generated mice with deletions of both Presenilin1 and Presenilin2 genes, the only genes encoding Presenilin in the mouse genome. To target Notch inactivation specifically to developing T cells, we introduced Cd4-Cre to mediate Presenilin gene deletion in a tissue- and stage-specific manner. Direct target genes of Notch signaling are largely unknown, and are likely to be cell lineage and stage specific. Therefore in order to identify potential Notch target genes , we compared RNA of thymocytes at the CD4+CD8+ stage of development from H-2b transgenic 5CC7 TCR/ RAG2-deficient / Presenilin1flox/flox /PS2-/- mice, with and without Cd4-Cre. Keywords: presenilin, thymocytes, mouse
2007-09-14 | GSE6590 | GEO
Project description:Regulation of presenilin genes. Presenilins are intramembrane aspartic proteases. These proteases are critical proteins in pathogenesis of Alzheimer's disease. The function of recently identified presenilin-homologous proteases (IMPAS or SPP)s is unknown. Our preliminary data in C.elegans model suggested the role of these proteins in early-development and , perhaps, in pathway related- to cholesterol -regulated signalling (Grigorenko et al, 2004, PNAS). The overall goal is to determine pattern of gene expression alterations in cells with knock-out or knock-down presenilin related proteins (IMPAS). The cultured cells, C.elegans and mouse models are planned to be used in this study. Here , we will determine gene expression patterns in C.elegans strain NL2099, fed with bacteria HT115, producing dsRNA for Ce-imp-2 gene (knock-down of imp-2 gene by RNAi )or GFP gene as a control. We hypothesize that novel family of presenilin-related proteases is important for cholesterol-regulated intracellular signalling and early development (including CNS/neuronal development and function). C.elegans (strain NL2099) on L1 stage were placed on agarose plates with bacteria HT115, producing dsRNA for: 1) Ce-imp-2 gene; 2) GFP as a control gene. After 48 hours at 20C , worms were washed in M9 buffer and total RNA was isolated by TRIzol method. Keywords: dose response
2007-03-23 | GSE7354 | GEO