Exposure to particulate matter (PM) pollution has direct impacts on the respiratory organs. However, the molecular alterations underlying PM-induced pulmonary injury remain unclear. In this study, we aimed to investigate the effects and pathomechanism of PM in lungs.
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus Rattus (black Rat)
SUBMITTER: Chia-Li Han
PROVIDER: PXD020265 | JPOST Repository | Mon Jul 27 00:00:00 BST 2020
REPOSITORIES: jPOST
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Project description:T cells undergo autoimmunization following spinal cord injury (SCI) and play both protective and destructive roles during the recovery process. T-cell deficient athymic nude (AN) rats recover better than immunocompetent Sprague-Dawley (SD) rats following spinal cord transection. In the present study, we evaluated locomotor recovery in SD and AN rats following moderate spinal cord contusion. To explain variable locomotor outcome, we assessed whole-genome expression using RNA sequencing, in the acute (1 week post-injury) and chronic (8 weeks post-injury) phases of recovery. AN rats demonstrated greater locomotor function than SD rats only at 1 week post-injury, coinciding with peak T cell infiltration in immunocompetent rats. Genetic markers for T cells and helper T cells were acutely enriched in SD rats, while AN rats expressed genes for Th2 cells, cytotoxic T cells, NK cells, mast cells, IL-1a, and IL-6 at higher levels. Acute enrichment of cell death-related genes suggested that SD rats undergo secondary tissue damage from T cells. Additionally, SD rats exhibited increased acute expression of voltage-gated potassium (Kv) channel-related genes. However, AN rats demonstrated greater chronic expression of cell death-associated genes and less expression of axon-related genes. We put forth a model in which T cells facilitate early tissue damage, demyelination, and Kv channel dysregulation in SD rats following contusion SCI. However, compensatory features of the immune response in AN rats cause delayed tissue death and limit long-term recovery. T cell inhibition combined with other neuroprotective treatment may thus be a promising therapeutic avenue. 2x2 model with 4 groups and 12 total samples. 2 rat strains (athymic nude [AN] and Sprague-Dawley [SD]) and 2 time points (1 week post-injury [acute] and 8 weeks post-injury [chronic]). 3 samples per group, for a total of 12 samples. No technical replicates were performed. Acute SD group = rats 618, 619, and 620. Chronic SD group = rats 605, 606, and 608. Acute AN group = rats 714, 715, and 717. Chronic AN group = rats 707, 712, and 713.
2015-10-26 | E-GEOD-62760 | biostudies-arrayexpress
Project description:Drug addiction is a chronic relapsing brain disease. The alterations of glucose uptake and metabolism were found in the brain of drug addicts. Insulin mediates brain glucose metabolism and its abnormality could induce brain injury and cognitive impairment. Here, we established a rat model of phenobarbital addiction by 90 days dosed escalation and evaluated addiction-related symptoms. We also performed proteomic analysis of the function of the differentially expressed (DE) proteins via bioinformatics in brain tissues by LC-MS/MS on day 60 and 90 of phenobarbital or 0,5% CMC-Na (vehicle) administration. The results showed that phenobarbital addictive rats developed severe withdrawal symptoms after abstinence. Proteomics analysis showed that numerous DE proteins were enriched after phenobarbital administration; which CALM1, ARAF and Cbl proteins (related to insulin signaling pathway) were significantly downregulated on day 60 but no day 90; however, SLC27A3 and NF-kB1 proteins (related to insulin resistance) were significantly upregulated on day 90. Our data indicate that insulin signaling pathway and insulin resistance may play a role in the development of phenobarbital addiction and brain injury and the findings may have important clinical implication.
2020-10-29 | PXD021101 | Pride
Project description:We conducted a calculi rat model, applied for an integrated proteomic and transcriptomic analysis to characterize the distinct gene expression profiles in calculi oxalate stone formation and its related kidney injury. Six distinct gene clusters were identified according to the consistency of transcriptome and proteome. Gene Ontology and KEGG pathway enrichment was performed to analyze the functions of each sub-group differentially expressed genes. Results showed that the calculi rat kidney was increased expression of injured & apoptotic markers and immune-molecules, and decreased expression of solute carriers & transporters and many metabolic related factors. The present proteotranscriptomic study provided a data resource and new insights for better understanding of the pathogenesis of nephrolithiasis, will hopefully facilitate the future development of new strategies for the recurrence prevention and treatment in patients with kidney stone disease.
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Project description:The rat tendon injury models were established and divided into three groups: normal control group, injury model group, and celecoxib + lactoferrin treatment group. Then, RNA sequencing and differential expression analysis were performed for samples from injury model group and celecoxib + lactoferrin treatment group on day 14. Next, autophagy/hypoxia/ferroptosis/pyroptosis-related genes retrieved from the corresponding databases and related literatures were downloaded to obtain the genes associated with autophagy/hypoxia/ferroptosis/pyroptosis. Subsequently, functional annotation, protein-protein interaction (PPI) network and transcriptional regulatory network construction for these genes were performed.
2022-11-20 | GSE201161 | GEO
Project description:Aim: To find the genes that related with the drug's(7-P) function. Design: 36 Rats were randomly divided into three group:control group(12), model group(12) and drug group(12). At last, randomly choosing 3 Rat from each group to do genechip analysis. In model group, the Porcine serum was given intraperitoneally (i.p.) to rats in a volume of 1.5 mL/kg every 3 days for a total of 20 treatments. Effect on model animals was confirmed by liver histology and biochemical assays . In drug group, 7-P was dissolved in balanced saline solution for administration subcutaneously at dosages of 174 μg/kg in a volume of 1 mL/kg. The doses were given 15 times, one day interval. In control group, the animals were not treated with porcine serum. but given an equal volume of vehicle alone. During 7-P and vehicle administration, porcine serum was given intraperitoneally (i.p.) to rats in a volume of 1.5 mL/ kg once weekly. All animals were fasted for 24 h before porcine serum treatment. Background: During investigation of hypervariable region 1 (HVR1) of hepatitis C virus (HCV), a seven amino acids mimic peptide named 7-P was identified within the N-terminal of HVR1 that could induce IFN-γ and IL-10 expression while decreasing the expression of TNF-α in vivo and in vitro. Further studies revealed that 7-P could not only decrease the serum levels of aminotransferases (ALT, AST), alkaline phosphatase (AKP), and billirubin, but were also effective in reversing histopathological evidence of inflammation-mediated hepatic injury in 3 rat models. The protective mechanism and gene expression profiles were investigated in detail in a rat chronic liver injury model using Affymetrix microarrays . Conclusion: We found that IL-1β, tumor necrosis factor receptor superfamily 14 (TNFRSF14), intercellular adhesion molecule 2 (ICAM2), sterol regulatory element-binding protein 1 (SREBP 1), Prohibitin (PHB), and inhibitor of DNA binding 2 (Id2) were the target genes that related with 7-P Keywords: comparative genomic hybridization 36 Rats were randomly divided into three group:control group(12), model group(12) and drug group(12). At last, randomly choosing 3 Rat from each group to do genechip analysis.
2009-09-30 | E-GEOD-10669 | biostudies-arrayexpress
Project description:Heat illness, which remains an occupational and environmental hazard, can be caused by excessive strain or heat load in combination with other factors. In the 10-year period from 1999 to 2009, an average of 658 annual heat-related deaths occurred in the United States. While heat stress at the cellular level has been studied, a paucity of risk assessment and injury biomarkers as well as therapeutic interventions remains. To identify novel biomarkers and to further understand the molecular mechanisms of heat stress, we identified differentially expressed microRNAs (miRNAs) in the heart, liver, and kidney from a conscious rat model at three time points. We distinguished the effect in animals with histopathological evidence of heart injury from those without evidence of organ injury. In animals without evidence of injury, we identified a total of 45 unique modulated miRNAs, whereas in the three animals with evidence of injury, we identified 171 unique differentially expressed miRNAs. The majority of the perturbed miRNAs were both time and tissue specific. Using the data from a microarray companion study, we identified the mRNAs that are the predicted targets of the differentially expressed miRNAs and performed pathway enrichment analysis. The enrichment analysis suggested that the perturbed miRNAs are involved in biological pathways related to energy metabolism, the unfolded protein response, and organ injury. These miRNAs may serve as organ-specific heat stress biomarkers of exposure or effect, as well as identify potential targets of heat illness prevention. Heart, liver, lung and kidney tissue was collected from rats at Tc,max and at 24 and 48 h for both heat exposed rats (n=4 to 6) or time matched, unheated controls (n= 4 to 6)
2016-08-10 | E-GEOD-81331 | biostudies-arrayexpress
Project description:Traumatic brain injury occasionally causes posttraumatic epilepsy. To elucidate the molecular events responsible for posttraumatic epilepsy, we established a rodent model that involved the injection of microliter quantities of FeCl3 solution into the amygdalar nuclear complex. We previously compared hippocampal gene expression profiles in the traumatic epilepsy model and normal rats at 5 days after brain injury (acute phase) and observed the role of inflammation. In this study, we focused on later stages of epileptogenesis. We compared gene expression profiles at 5, 15 (sub-chronic phase), and 30 days (chronic phase) after brain injury to identify temporal changes in molecular networks involved in epileptogenesis. A total of 81 genes was significantly (at least 2-fold) up- or downregulated over the course of disease progression. We found that genes related to lipid metabolism, namely, Apoa1, Gh, Mc4r, Oprk1, and Pdk4, were temporarily upregulated in the sub-chronic phase. Changes in lipid metabolism regulation might be related to seizure propagation during epileptogenesis. This temporal description of hippocampal gene expression profiles throughout epileptogenesis provides clues to potential markers of disease phases and new therapeutic targets. We employed amygdalar FeCl3 injection to induce chronic, recurrent limbic-type partial seizures with spontaneous secondarily generalized seizures in rats . Sixteen male Wistar rats were kept in hanging cages with unlimited access to food and water and 12-h light-dark cycles. Surgical procedures were conducted following anesthesia with intraperitoneal (i.p.) sodium pentobarbital injections (37.5 mg/kg) at 5 weeks of age. Stereotaxic coordinates were determined with the rat brain atlas. The incisor bar was set 3.3 mm below the interaural line. While under anesthesia, a polyethylene tube containing a stylet to serve as an external guide cannula (1.09-mm outer diameter (o.d.), 0.55-mm inner diameter (i.d.), 2.5 cm in length) was stereotaxically implanted and anchored to the skull with miniature screws and dental cement. The cannula was fixed 5.6 mm anterior and 4.8 mm to the right of the lambda and 8.5 mm below the surface of the skull, positioning it at the right amygdaloid body. Randomly selected rats for in vivo microdialysis to estimate redox had guide cannula placed but were prepared without dental cement on the skull where the microdialysis guide cannula was to be placed. Five days later, the stylet was replaced with an internal delivery cannula (0.5 mm o.d., 0.25 mm i.d.). FeCl3 was dissolved in saline solution (100 mM, pH 2.2). FeCl3 solution (1.0 M-NM-<l) was injected through the inner cannula by means of a microinfusion pump (EP-60; Eicom, Tokyo, Japan) set at a rate of 1.0 M-NM-<l/min (Fe group; n = 12). The external guide cannula was used for electroencephalogram (EEG) recording with an electroencephalograph (type 1A63; SAN-EI, Tokyo, Japan). Rats in the control group (n = 4) were each injected with 1.0 M-NM-<l saline (pH 2.2). Both EEG and behavior were observed for at least 6 h after the injection. While we did not measure the rate or frequency of seizures, we did confirm that the animals had recurrent seizures. These observations and the acute recording confirmed the accuracy of the amygdalar injection. No seizure activity was observed in control group rats. Animals in the control group were sacrificed by cervical dislocation 15 days after amygdalar injection. Animals in the Fe group were subdivided into 3 groups and were sacrificed at 5 (acute phase), 15 (sub-chronic phase of injury), and 30 days (chronic phase of injury) after amygdalar injection. The stages of disease development were categorized according to the EEGs of the model rats; within 5 days after amygdalar injection, epileptiform discharges were recorded in the contralateral and ipsilateral amygdalae; by 15 days after injection, interictal spike discharges were more consistently observed in the contralateral uninjected amygdala; at 30 days after injection bilateral interictal spike discharges continued to be observed. After sacrifice, the right hippocampi were immediately removed and placed in ice-cold phosphate-buffered saline and homogenized (Polytron PT 3000; Brinkmann Instruments, Inc., Westbury, NY, USA) for RNA extraction.
2012-12-31 | E-GEOD-40490 | biostudies-arrayexpress
Project description:Aim: To find the genes that related with the drug's(7-P) function. Design: 36 Rats were randomly divided into three group:control group(12), model group(12) and drug group(12). At last, randomly choosing 3 Rat from each group to do genechip analysis. In model group, the Porcine serum was given intraperitoneally (i.p.) to rats in a volume of 1.5 mL/kg every 3 days for a total of 20 treatments. Effect on model animals was confirmed by liver histology and biochemical assays . In drug group, 7-P was dissolved in balanced saline solution for administration subcutaneously at dosages of 174 μg/kg in a volume of 1 mL/kg. The doses were given 15 times, one day interval. In control group, the animals were not treated with porcine serum. but given an equal volume of vehicle alone. During 7-P and vehicle administration, porcine serum was given intraperitoneally (i.p.) to rats in a volume of 1.5 mL/ kg once weekly. All animals were fasted for 24 h before porcine serum treatment. Background: During investigation of hypervariable region 1 (HVR1) of hepatitis C virus (HCV), a seven amino acids mimic peptide named 7-P was identified within the N-terminal of HVR1 that could induce IFN-γ and IL-10 expression while decreasing the expression of TNF-α in vivo and in vitro. Further studies revealed that 7-P could not only decrease the serum levels of aminotransferases (ALT, AST), alkaline phosphatase (AKP), and billirubin, but were also effective in reversing histopathological evidence of inflammation-mediated hepatic injury in 3 rat models. The protective mechanism and gene expression profiles were investigated in detail in a rat chronic liver injury model using Affymetrix microarrays . Conclusion: We found that IL-1β, tumor necrosis factor receptor superfamily 14 (TNFRSF14), intercellular adhesion molecule 2 (ICAM2), sterol regulatory element-binding protein 1 (SREBP 1), Prohibitin (PHB), and inhibitor of DNA binding 2 (Id2) were the target genes that related with 7-P Keywords: comparative genomic hybridization
2009-09-30 | GSE10669 | GEO
Project description:A rat model of skeletal muscle mechanical compression injury was established with varying degrees of injury severity, one control group, and two compression groups (Mild Injury and Severe Injury Group). LC-MS/MS-4D-DIA quantitative proteomics technology was employed to detect the plasma protein expression profiles of rats in different injury groups.
2025-05-07 | PXD052469 | Pride
Project description:Recently, thousands of cases of E-cigarette or vaping product use-associated lung injury (EVALI) were reported. But the lung toxicity of each E-cigarette components were still poorly defined. Major components of E-cigarette were nicotine, flavoring, vitamin E acetate (VEA), propylene glycol (PG) and vegetable glycerin (VG). In our previous study, we determine the different lung injury patterns in PG and VEA exposed mice; fibrotic injury in PG and asthmatic injury in VEA. In this study, we performed the transcriptomic analysis that could reflect different lung injury patterns caused by PG and VEA in lung tissues using RNS-Sequencing and bioinformatics tools. A combination of P-value <0.05 and fold change ≥1.5 was used to identify differently expressed genes (DEGs). Gene-expression data showed different gene-alteration patterns in the PG and VEA groups. Supervised analysis revealed that 1,193 PG and 1,795 VEA induced-specific genes, and functional analysis revealed that PG-specific genes were involved in TNC-related chronic obstructive pulmonary diseases, whereas VEA-specific genes were involved in asthma-related chronic lung injury. The results of transcriptomic analysis were consistent with lung histopathology results. These findings indicated that E-cigarette component-specific changes in gene expression closely reflected E-cigarette component pathological changes in E-cigarette component-induced lung injury.
2023-05-01 | GSE215850 | GEO