Mus musculus strain:Male(C57/B6N) Female (ICR)
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB16197 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR491671.fastq.gz | Fastqsanger.gz | |||
| DRR491672.fastq.gz | Fastqsanger.gz | |||
| DRR491673.fastq.gz | Fastqsanger.gz | |||
| DRR491674.fastq.gz | Fastqsanger.gz | |||
| DRR491675.fastq.gz | Fastqsanger.gz |
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Project description:Ischemic stroke is a major cause of death and disability worldwide. Translation into the clinical setting of neuroprotective agents showing promising results in pre-clinical studies has systematically failed. One of the reasons that could explain this failure is that the animal models used to test neuroprotectants do not represent properly the population affected by stroke, as the majority of pre-clinical studies are performed in healthy young male mice. In this regard, we aimed to determine if the response to cerebral ischemia differed depending on age, sex and the presence of comorbidities. Thus, we explored proteomic and transcriptomic changes triggered during the hyperacute phase of cerebral ischemia (by transient intraluminal middle cerebral artery occlusion) in the brain of: (1) young male mice, (2) young female mice, (3) aged male mice and (4) diabetic young male mice. Moreover, we compared the proteomic and transcriptomic changes of each group using an integrative enrichment pathways analysis to disclose key common and exclusive altered proteins, genes and pathways in the first stages of the disease. We found 61 differentially expressed genes (DEG) in male mice, 77 in females, 699 in diabetic and 24 in aged mice. Of these, only 14 were commonly dysregulated in all four groups. The enrichment pathways analysis revealed that the inflammatory response was the biological process with more DEG in all groups of animals, followed by hemopoiesis and lymphoid organ development. Our findings indicate that the response to cerebral ischemia regarding proteomic and transcriptomic changes differs depending on the sex, age and comorbidities, highlighting the importance of incorporating these groups of animals in future stroke research studies.
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Project description:BackgroundA broad suite of bisphenol S (BPS) derivatives as alternatives for BPS have been identified in various human biological samples, including 4-hydroxyphenyl 4-isopropoxyphenylsulfone (BPSIP) detected in human umbilical cord plasma and breast milk. However, very little is known about the health outcomes of prenatal BPS derivative exposure to offspring.ObjectivesOur study aimed to investigate the response of hepatic cholesterol metabolism by sex in offspring of dams exposed to BPSIP.MethodsPregnant ICR mice were exposed to 5μg/kg body weight (BW)/day of BPSIP, BPS, or E2 through drinking water from gestational day one until the pups were weaned. The concentration of BPSIP, BPS, or E2 in the plasma and liver of pups was determined by liquid chromatography-tandem mass spectrometry. Metabolic phenotypes were recorded, and histopathology was examined for liver impairment. Transcriptome analysis was employed to characterize the distribution and expression patterns of differentially expressed genes across sexes. The metabolic regulation was validated by quantitative real-time PCR, immunohistochemistry, and immunoblotting. The role of estrogen receptors (ERs) in mediating sex-dependent effects was investigated using animal models and liver organoids.ResultsPups of dams exposed to BPSIP showed a higher serum cholesterol level, and liver cholesterol levels were higher in females and lower in males than in the controls. BPSIP concentration in the male liver was 1.22±0.25 ng/g and 0.69±0.27 ng/g in the female liver. Histopathology analysis showed steatosis and lipid deposition in both male and female offspring. Transcriptome and gene expression analyses identified sex-specific differences in cholesterol biosynthesis, absorption, disposal, and efflux between pups of dams exposed to BPSIP and those in controls. In vivo, chromatin immunoprecipitation analysis revealed that the binding of ERα protein to key genes such as Hmgcr, Pcsk9, and Abcg5 was attenuated in BPSIP-exposed females compared to controls, while it was enhanced in males. In vitro, the liver organoid experiments demonstrated that restoration of differential expression induced by BPSIP in key genes, such as Hmgcr, Ldlr, and Cyp7a1, to levels comparable to the controls was only achieved when treated with a combination of ERα agonist and ERβ agonist.DiscussionFindings from this study suggest that perinatal exposure to BPSIP disrupted cholesterol metabolism in a sex-specific manner in a mouse model, in which ERα played a crucial role both in vivo and in vitro. Therefore, it is crucial to systematically evaluate BPS derivatives to protect maternal health during pregnancy and prevent the transmission of metabolic disorders across generations. https://doi.org/10.1289/EHP14643.
| S-EPMC11412574 | biostudies-literature