Whole genome resequencing of spleen in mice model
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE186567 | GEO | 2026/03/31
REPOSITORIES: GEO
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Project description:The perinatal period and early infancy are considered critical periods for lung development, and adversities during this period are believed to impact lung health in adulthood.The main factors affecting postnatal lung development and growth include environmental exposures, cigarette smoking, (viral) infections, allergic sensitization, and asthma.Therefore, we hypothesized that concomitant exposure in the early postnatal period in mice would cause more profound alterations in lung alveolarization and growth in adult life, quantified by stereology, and differently modulate lung inflammation and gene expression than either insult alone.Five-day-old male mice were immunized intraperitoneally (i.p.) with 10 µg of ovalbumin (OVA). This procedure was repeated at the 7th day of life, animals from the control group received i.p. injection of PBS only. Mice were exposed to either ambient PM2.5 or filtered air from the 5th to the 39th day of life, using an ambient particle concentrator developed at the Harvard School of Public Health (HAPC).Total RNA of lung samples (n=3 animals per group) was extracted using RNeasy Mini Kit (Qiagen, Hilden, Germany), according to manufacturer's instructions. The microarray analysis was performed using three RNA samples for each studied group (Control, OVA, PM2.5, OVA+PM2.5), totalizing 12 samples. One hundred nanograms of total RNA was amplified with the Ambion WT Expression Kit and hybridized onto the GeneChip Mouse Gene 2.0 ST Array (Thermo Scientific, Massachusetts, USA), following manufacturer’s protocol. The comparison between the control and OVA group exhibit 32 DEGs (28 up-regulated and 4 down-regulated), between the control and PM2.5 group had 6 DEGs (4 up and 2 down) and between the control and OVA+PM2.5 group had 5 DEGs (4 up and 1 down). The comparison between OVA and PM2.5 group showed 97 DEGS (22 up and 75 down) and between OVA and OVA+PM2.5 group had 7 DEGs (4 up and 3 down). Finally, the comparison between the PM2.5 and OVA+PM2.5 group exhibit 34 DEGs (2 up and 32 down).Our experimental data provide pathological support for the hypothesis that either allergic or environmental insults in early life have permanent adverse consequences to lung growth. In addition, combined insults were associated with the development of a COPD-like phenotype in young adult mice.
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Project description:In this study we investigated whether nicotinamide mononucleotide (NMN) could protect against Doxorubicin-induced cardiotoxicity and physical dysfunction in vivo. To assess the short- and long-term toxicity, two Doxo regimens were tested, acute and chronic. In the acute study, C57BL6/J (B6) mice were injected intraperitoneally (i.p.) once with Doxo (20 mg/kg) and NMN (180 mg/kg/day, i.p.) was administered daily for five days before and after the Doxo injection. In the chronic study, B6 mice received a cumulative dose of 20 mg/kg Doxo administered in fractionated doses for five days. NMN (500 mg/kg/day) was supplied in the mice’s drinking water beginning five days before the first injection of Doxo and continuing for 60 days after.
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Project description:Mucuna pruriens extract MPE pretreatment may have a direct protective effect on heart (other than immunological neutralization of the venom neurotoxin and phospholipase A2 by the anti-MPE antibodies) that renders the heart more resistant to the toxic action of the venom The direct protective effect probably involves functional changes to the cardiac tissue that enable the heart to resist the reduction of contractility and rate induced by the cobra venom.To explore the possibility of the direct action of MPE pretreatment on heart and to understand the molecular events involved in the protection of MPE pretreatment against the lethal action of Naja sputatrix venom, gene expression studies were carried out using microarray analysis. Rats were divided into four groups (n=6): negative control (abbreviated as ‘negative’ group), MPE pretreated group (abbreviated as ‘MPE’ group), N. sputatrix venom-challenge group (abbreviated as ‘NS’ group) and N. sputatrix venom-challenge to MPE pretreated animals group (abbreviated as ‘MPE-NS’ group). In the ‘MPE’ group, rats were injected with MPE at a dose of 21 mg/kg (i.p.), on day 0, 7 and 14, and sacrificed on day 21. In the ‘negative’ group (the untreated, control group), rats were injected with saline of the same volume and sacrificed also on day 21. Hearts were then harvested immediately. In the N. sputatrix venom-challenge group (‘NS’ group), untreated rats were challenged with 1.5 LD50 (1.25 ?g/g) of N. sputatrix venom whereas in the venom challenge to MPE pretreated animals group (the ‘MPE-NS’ group), MPE pretreated rats were challenged with 1.5 LD50 (1.25 ?g/g) of N. sputatrix venom, both on day 21. For the ‘NS’ and ‘MPE-NS’ group, the rats were observed for 24 h after venom challenged and hearts were harvested as soon as death occurred or 24 h after the venom injection, whichever occurred first.
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Project description:Asthma is a chronic inflammatory airway disease characterized by airway hyperresponsiveness and remodeling. In this study, we aimed to investigate the transcriptomic changes in the lung tissue of asthmatic mice using a well-established ovalbumin (OVA)-induced asthma model. Female BALB/c mice (6-8 weeks old) were randomly divided into two groups: sham (n=6) and OVA (n=5). The OVA group received intraperitoneal injections of 20 μg OVA and 2 mg Al(OH)₃ on days 0 and 14. Subsequently, from day 21 to day 23, the mice were exposed to 1% OVA aerosol for 30 minutes each day. The sham group received an equivalent volume of vehicle. After 24 hours of the last aerosol exposure, the mice were sacrificed, and lung tissues were collected for RNA sequencing. The sequencing data were analyzed to identify differentially expressed genes and pathways associated with asthma development and progression. The results provide valuable insights into the molecular mechanisms underlying OVA-induced asthma and may identify potential therapeutic targets.
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Project description:cDNA microarray study of gene expression changes in whole blood from LPS treated rats, 2 and 6 hours after I.P. injection of 5 mg/kg Keywords: time-course
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Project description:The primary objective of this study was to investigate the imapcts of maternal exposure to CBD on offsrping cardiac function and to gain mechanistic insights underlying the functional impacts. Pregnant rats were randomly assigned to a treatment group; (1) vehicle control, (2) 3 mg/kg/day or (3) 30 mg/kg/day i.p. CBD from gestational day 6-22. Primary findings indicate that excusively male offsrping exhibit impaired cardiac function. The primary findings in the heart transcriptome data indicates several GO terms suggesting altered pathways involving mitochondrial metabolism and developmental pathways.
2023-09-20 | GSE242079 | GEO
Project description:The present study was designed using MT knockout mice in concert with genomic approaches to explore the possible molecular and cellular mechanisms involved in the protective effects of MT against DOX cardiotoxicity. MT-M-bM-^EM- /M-bM-^EM-! null (MT-/-) mice and corresponding wild-type mice (MT+/+) were administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of saline. Animals were sacrificed on the 4th day after DOX administration and samples were collected for further analyses. Global gene expression profiles of cardiac mRNA from two genotype mice revealed that 381 characteristically MT-responsive genes were identified between MT+/+ mice and MT-/- mice in response to DOX, including fos, ucp3, car3, atf3, map3k6, etc.. Functional analysis implied MAPK signaling pathway, p53 signaling pathway, Jak-STAT signaling pathway, PPAR signaling pathway, Wnt signaling pathway, etc. might be involved to mediate the protection of DOX cardiomyopathy by MT. Results from the present study not only validated the previously reported possible mechanisms of MT protection against DOX toxicity, but also provided new clues into the molecular mechanisms involved in this process. Male MT+/+ & MT-/- mice (6-8 weeks old) were randomly assigned to treatment or control groups and administrated with a single dose of DOX (15 mg/kg, i.p.) or an equal volume of normal saline solution (NS) respectively. Animals were sacrificed on the 4th day after DOX injection, and samples were collected for further microarray analyses.
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