Effects of PAMAM dendrimers in the mouse brain after a single intranasal instillation
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE56159 | GEO | 2014/03/26
SECONDARY ACCESSION(S): PRJNA242608
REPOSITORIES: GEO
Similar Datasets
Project description:The in vivo effects of nasal exposure to polyamidoamine (PAMAM) dendrimers on their effects on gene expression in the mouse brain. A single dose of PAMAM dendrimers or saline (control) was intranasally administered to 8-week old male BALB/c mice. PAMAM-induced gene expression in the olfactory bulb, hippocampus, and cerebral cortex was measured at 24 hours after exposure to doses of 0, 0.15 mg/kg b.w. Pooled RNA from six independent experiments were analyzed at each time.
2014-03-26 | E-GEOD-56159 | biostudies-arrayexpress
Project description:Intra-tracheal instillation of saline or PM2.5 was performed in BALB/c Mice once a week for consecutive eight weeks. Genomewide transcriptome profiling of coding genes, long non-coding RNAs (lncRNA), and circular RNAs (circRNA) in mice lung were done by ribosomal RNA-depleted RNA sequencing.
2020-01-01 | GSE132572 | GEO
Project description:Interventions: insulin group (group I):Starting two days before surgery, insulin nasal drops should be administered twice a day until the day of surgery, 20U each time (0.5 ml) ;control group (group C):Starting two days before surgery, physiological saline nasal drops of 0.5 ml were administered twice a day until the day of surgery
Primary outcome(s): The incidence of postoperative cognitive dysfunction
Study Design: Parallel
| 105486 | ecrin-mdr-crc
Project description:Microarray analysis of whole lung tissue from three mouse models of asthma Acute asthma was produced by immunization twice, one week apart, of Balb/C mice 8-12 weeks of age with Aspergillus species (5 μg) in adjuvant (1:1 vol/vol). Adjuvant was aluminum and magnesium hydroxide (Pierce). Asthma was initiated by three consecutive intranasal exposures to Aspergillus species (5μg in 15μL saline) and asthma was evaluated 72 hours after the final exposure. Tolerant asthma was produced by intranasal delivery of Aspergillus species (5μg in 15μL saline) twice a week for six consecutive weeks to Balb/C mice 8-12 weeks of age. Asthma was evaluated after mice were rested for an additional three weeks. Chronic asthma was produced by intranasal delivery of the Dustmite/ Ragweed/ Aspergillus (5,50,5ug in 15ul saline) mixture twice a week for six consecutive weeks in female mice Balb/C mice 8-12 weeks of age. Asthma was evaluated 3 weeks after cessation of allergen exposure. Saline control mice were treated intransally with 15ul of saline twice a week for 6 weeks. Asthma was assesed 3 weeks after the final exposure.
2014-02-15 | GSE54297 | GEO
Project description:Purpose: The goal of this study is to address if in utero and early life nicotine exposure can prime the offspring to be more succetible to develop emphysema in adulthood Methods: A mouse model of two hits: a prenatal hit and a later insult delivered in adulthood was used in this study. In brief, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and until the post-natal day 16 (nicotine group). As a control, we used drinking water with 2% saccharin (control group). Pups born from nicotine-exposed or control mothers were intranasally instilled with elastase or saline at the age of 11 weeks and sacrificed at post-elastase day (ped) 21. Lungs were collected at ped21 and laser dissected to separate the emphysematous and normal-looking tissue from elastase-instilled lungs. The RNA was then extracted and submited to RNAseq analysis. We had 6 different groups: two for saline instilled animals (normal_control_saline (C-S), normal_nicotine-saline (N-S)), and for elastase-instilled animals we had 4 groups: 2 for emphysematous regions (emphysema_ControlElastase (eC-E) and emphysema_NicotineElastase(eN-E)) and 2 for normal regions (normal_ControlElastase(nC-E) and normal_NicotineElastase(nN-E)). Results: Nicotine upregulated zero and 46 genes and downregulated 2 and 29 in saline and elastase instilled respectivelly. Elastase upregulated zero and 3 and downregulated 1 and 1 genes in controls and nicotine-pretreated samples respectively. Pathway analysis performed with differentially expressed genes due to nicotine-pretreatment in elastase instilled animals with MetaCore software (https://portal.genego.com/) (fold change of 2 or more and p<0.05) revealed downregulation of the several immune system related pathways, gamma-secretase proteolitic pathway, ubiquitin-proteasomal pathway, notch signaling pathway and others. Conclusions: Our results identify the the early nicotine exposure as an important insult that affects the proteomic signature at ped21
2022-03-09 | GSE167568 | GEO
Project description:Polyinosinic:polycytidylic acid (poly I:C) is a synthetic analogue of double-stranded (ds)RNA, a molecular pattern associated with viral infections, that is used to exacerbate inflammation in lung injury models. Despite its frequent use, there are no detailed studies of the responses elicited by a single topical administration of poly I:C to the lungs of mice. Our data provides the first demonstration that the molecular responses in the airways induced by poly I:C correlate to those observed in the lungs of COPD patients. These expression data also revealed three distinct phases of response to poly I:C, consistent with the changing inflammatory cell infiltrate in the airways. Poly I:C induced increased numbers of neutrophils and NK cells in the airways, which were blocked by CXCR2 and CCR5 antagonists, respectively. Using gene set variation analysis on representative data sets, gene sets defined by poly I:C-induced DEGs were enriched in the molecular profiles of chronic obstructive pulmonary disease (COPD), but not idiopathic pulmonary fibrosis patients. Collectively, these data represent a new approach for validating the clinical relevance of preclinical animal models and demonstrate that a dual CXCR2/CCR5 antagonist may be an effective treatment for COPD patients. Temporal genomic characterization of lung homogenate from male BALB/cJ mice treated intranasally with poly I:C or saline was carried out at 7 timepoints post poly I:C/saline adiministration (2, 6, 24, 48, 72, 96, 168 hours). Mice were anesthetized with isoflurane and intranasally (i.n.) administered saline or poly I:C (InvivoGen, San Diego, CA) at a sub-maximal dose of 30 µg in 50 µl sterile saline. For time course studies, the 30 µg was administered i.n. once and assessed from 2 – 168 hours. Total RNA was isolated from the mouse lung tissue of poly I:C and saline treated mice across 7 time points (2, 6, 24, 48, 72, 96, and 168 hours, n=6 per group) and homogenized in QIAzol reagent. Purified total RNA was amplified and labeled using NuGen Ovation kits (NuGEN Technologies, Inc., San Carlos, CA) and RNA from samples was hybridized to Affymetrix Mouse 430 2.0 arrays.
2013-02-27 | E-GEOD-39304 | biostudies-arrayexpress
Project description:House dust mite (HDM) extract (Greer Laboratories, Lenoir, NC) was resuspended in sterile phosphate-buffered saline (PBS) at a concentration of 0.5 mg (protein)/ml and 10 ul (5 ug dose) was administered to isofluorane-anesthetized mice intranasally. Groups of mice were infected either with influenza A or exposed to PBS. Seven days later, separate groups of mice were either exposed to saline or HDM for 3 or 6 days and lungs harvested 24 h after the last exposure, at day 4 (early phase; EP) or day 7 (late phase; LP).
2011-08-16 | E-MEXP-3325 | biostudies-arrayexpress
Project description:Purpose: The goal of this study is to address if in utero and early life nicotine exposure can affect genetic profile in early ephysema Methods: A mouse model of two hits: a prenatal hit and a later insult delivered in adulthood was used in this study. In brief, Nicotine (200 mg/L) was supplied immediately after mating and administered to the females in drinking water supplemented with 2% saccharin for the whole period of gestation and until the post-natal day 16 (nicotine group). As a control, we used drinking water with 2% saccharin (control group). Pups born from nicotine-exposed or control mothers were intranasally instilled with elastase or saline at the age of 11 weeks and sacrificed at post-elastase day (ped) 3. Whole lung were collected at ped3 and total RNA was sequenced. We had 4 different groups: control_saline (C-S), control_elastase (C-E), nicotine_saline (N-S) and nicotine_elastase (N-E). ALl the groups had 3 replicas, except N-E group that had 5 different replicas. Results: At ped3 nicotine upregulated 219 and 2 and downregulated 2 and 109 genes in saline and elastase-instilled samples respectively. Elastase upregulated 723 and 439 and downregulated 116 and 77 genes in controls and nicotine-pretreated samples respectively. Pathway analysis performed with MetaCore software (https://portal.genego.com/) (fold change of 2 or more and p<0.05) revealed many identical pathway activated by elastase instillation in both controls and nicotine-pretreated samples such as the cell cycle, DNA damage and cell adhesion, but also revieled the main difference in activation of the immune system between the controls and nicotine-pretreated samples. Conclusions: Our results identify the the early nicotine exposure as an important insult that affects the proteomic signature at ped3
2022-03-09 | GSE167567 | GEO
Project description:Microarray analysis of whole lung tissue from three mouse models of asthma Acute asthma was produced by immunization twice, one week apart, of Balb/C mice 8-12 weeks of age with Aspergillus species (5 μg) in adjuvant (1:1 vol/vol). Adjuvant was aluminum and magnesium hydroxide (Pierce). Asthma was initiated by three consecutive intranasal exposures to Aspergillus species (5μg in 15μL saline) and asthma was evaluated 72 hours after the final exposure. Tolerant asthma was produced by intranasal delivery of Aspergillus species (5μg in 15μL saline) twice a week for six consecutive weeks to Balb/C mice 8-12 weeks of age. Asthma was evaluated after mice were rested for an additional three weeks. Chronic asthma was produced by intranasal delivery of the Dustmite/ Ragweed/ Aspergillus (5,50,5ug in 15ul saline) mixture twice a week for six consecutive weeks in female mice Balb/C mice 8-12 weeks of age. Asthma was evaluated 3 weeks after cessation of allergen exposure. Saline control mice were treated intransally with 15ul of saline twice a week for 6 weeks. Asthma was assesed 3 weeks after the final exposure. n=3 samples/ mouse model.
2014-02-15 | E-GEOD-54297 | biostudies-arrayexpress
Project description:To profile airway and parenchyma transcriptomes in our mouse model of asthma chronic obstructive pulmonary disease overlap, we employed RNA-Seq (TruSeq Stranded mRNA sample preparation, NovaSeq 6000, 20 million 100 bp single reads) as a discovery tool to identify mRNAs of interest in the development of experimental asthma chronic obstructive pulmonary disease overlap. Experimental asthma: Some mice were sensitized and challenged intranasally with house dust mite (HDM) extract 5 days per week for 3 weeks. In other mice, this was HDM treatment 3 times/week from weeks 4-11. Controls received phosphate buffered saline (PBS). Experimental chronic obstructive pulmonary disease (COPD): Mice were exposed to cigarette smoke (CS) twice per day, 5 days per week for 8 weeks. Control mice were exposed to normal air (AIR). Experimental asthma-COPD overlap (ACO): Mice were sensitized and challenged intranasally with HDM or PBS. From weeks 4-11, mice were also exposed to CS or AIR. Treatment with dexamethasone (DEX): Separate groups of mice were treated with DEX during week 11. Lungs were excised, airway and parenchyma tissue were isolated through blunt dissection, and total RNA isolated.
2023-02-01 | GSE199853 | GEO