Adrenal stress response is an essential host response against lethal T cell activation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA745198 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15090070_1.fastq.gz | Fastqsanger.gz | |||
| SRR15090070_2.fastq.gz | Fastqsanger.gz | |||
| SRR15090071_1.fastq.gz | Fastqsanger.gz | |||
| SRR15090071_2.fastq.gz | Fastqsanger.gz | |||
| SRR15090072_1.fastq.gz | Fastqsanger.gz |
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Project description:Cytokine release syndrome (CRS) is a major cause of death in lethal T cell activation and presents a significant barrier for CAR-T immunotherapy or allogenic hematopoietic cell transplantation. We reported here that adrenal stress response, defined by a 5-10-fold increase in induced glucocorticoid (iGC) production, is an essential host response against lethal T cell activation. We identified scavenger receptor BI (SR-BI), a HDL receptor, as a key regulator for iGC production. Using SR-BI null mice as an adrenal stress response deficiency model, we demonstrated that adrenal stress response protects anti-CD3 induced death through keeping CRS under control and relative adrenal insufficiency (RAI) – lacking adrenal stress response, is a risk factor.
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Project description:To gain insight into the adrenal stress response, we analyzed differential mRNA expression of genes associated with stress induced by aggressive behaviour in the pig In an animal experiment various levels of aggressive behaviour and stress were induced by mixing groups of unfamiliar pigs with different aggressiveness. To analyze adrenal stress response we selected two experimental groups for comparison, each comprising eight animals (n=16) which differed significantly in aggressive behaviour and plasma cortisol levels. To identify differentially expressed genes, we compared the adrenal transcriptome of these two groups of pigs, using the Affymetrix GeneChip porcine Genome Array.
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Project description:Transcription factor GATA6 is expressed in the fetal and adult adrenal cortex and has been implicated in steroidogenesis. To characterize the role of GATA6 in adrenocortical development and function, we generated mice in which Gata6 was conditionally deleted using Cre-LoxP recombination with Sf1-cre. The adrenal glands of adult Gata6 conditional knockout (cKO) mice were small and had a thin cortex with thickened capsule. Cytomegalic changes were evident in the adrenal glands of fetal and adult cKO mice, and chromaffin cells were ectopically located at the periphery of the glands. The secretion of corticosterone in response to exogenous ACTH was blunted in cKO mice. Cells expressing gonadal-like markers, including Gata4, Amhr2, and Tcf21, accumulated in the adrenal capsule and subcapsule of cKO mice, suggesting aberrant adrenocortical progenitor/stem cell differentiation. Gonadectomy triggered the overexpression of sex steroidogenic differentiation markers, such as Lhcgr and Cyp17, in the adrenal glands of male and female cKO mice. Nulliparous female and orchiectomized male cKO mice lacked an adrenal X-zone. Microarray hybridization identified Pik3c2g as a novel X-zone marker that is downregulated in the adrenal glands of nulliparous female Gata6 cKO mice. Our findings offer genetic proof of the longstanding hypothesis that GATA6 regulates the differentiation of steroidogenic progenitors into corticoid-producing cells. 3 replicates from both conditional knockout of Gata6 in the adrenal gland and control adrenal glands from non-knockout mice were compared
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Project description:Helicobacter pylori, a pathogenic member of phylum Campylobacterota (formerly Epsilonproteobacteria), is recognized as the leading cause of several human gastric pathologies, including acute and chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphoma. In the last two decades, the alarming increase of the antibiotic resistance levels to first-line and even “rescue” antibiotics, especially clarithromycin, metronidazole and levofloxacin, has led to a marked decrease of the eradication rates of traditional therapies. In previous works, we have validated the essential protein HsrA as an effective therapeutic target for H. pylori infection. HsrA is an OmpR/PhoB-type orphan response regulator, unique and highly conserved in members of phylum Campylobacterota, which appears involved in a variety of crucial physiological processes. In the present work, we carried out a transcriptomic analysis in order to discern the global effects of lethal concentrations of a bactericidal HsrA inhibitor on the H. pylori physiology. Treatment with the bactericidal HsrA inhibitor significantly changed the transcript levels of 367 open reading frames (ORF), of which 212 genes appeared upregulated and 155 genes resulted in downregulation, as compared with control samples. Thus, in vivo HsrA inhibition influenced, directly or indirectly, the expression of 23% of ORFs encoded by the H. pylori 26696 genome. Among the 268 differentially expressed genes (DEGs) with defined functions, two functional categories were highly enriched with downregulated genes involved in essential physiological processes: (1) ribosome biogenesis, and (2) electron transfer and oxidative phosphorylation.
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Project description:The extracellular matrix (ECM) comprises macromolecules that shape a complex three-dimensional network. Filling the intercellular space and playing a crucial role in the structure and function of tissues, ECM regulates essential cellular processes such as adhesion, differentiation, and cell signaling. In the human adrenal gland, composed of cortex and medulla surrounded by a capsule, the ECM has not yet been directly described, although its impact on the processes of proliferation and steroidogenesis of the adrenal cortex is recognized. This study proposes a comprehensive analysis aims to comprehensively analyze the ECM of the adult human adrenal cortex, which is separated into outer fraction (OF) and inner fraction (IF), by comparing their proteomic profiles. The study discusses the composition, spatial distribution, and relevance of differentially expressed ECM signatures of the adrenal cortex matrisome on adrenal structure and function. The findings were validated through database analysis (cross-validation), histochemical, and immunohistochemical approaches. A total of 121 ECM proteins were identified and categorized into glycoproteins, collagens, ECM regulators, proteoglycans, ECM-affiliated proteins, and secreted factors. Thirty-one ECM proteins were identified only in OF, 9 only in IF, and 81 were identified in common with both fractions. Additionally, 106 ECM proteins were cross-validated using Human matrisome DB 2.0 and the proteins differentially expressed in OF and IF, were identified. This study provides significant insights into the composition and regulation of the ECM in the human adrenal cortex, shedding light on the adrenal microenvironment and its role in the functioning, maintenance, and renewal of the adrenal gland.
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Project description:Transcriptomic analysis of Helicobacter pylori 26695 exposed to lethal concentration of a bactericidal inhibitor of the essential response regulator HsrA
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Project description:Stress leads to important adaptive physiological responses including release of catecholamine from the adrenal medulla. Repeated or prolonged stess increses the propensity for many disorders including cardiovascular disease and neuropsychiatric disorders. The susceptibility to stress is determined by a number of factors including prior experience with stress. It has been found that while there is adaptation to prolonged cold stres; it leads to sensitization when cold stressed animals are exposed to a different (novel) stressor. Our study aims to determine the mechanis of this adaptatio and sensitization. We will determine teh gene expression patterns in rat adrenal medulla in response to severa times of cold stress. We will also determine the changes in gene expresion with single immobilization stress in adrenal medulla of rat with an dwithout preexposure to cold stress to investigate the mechanism of sensitizatio in cold adapted animals. We hypothesize that during the course of cold stess there are alterations in gene expression of several neurotransmitter related genes and transcription factors. In expression of several trascription factors, such as Fra-2 which lead to an exaggerated response to teh novel stresor. Rats were exposed to cold stress (4 degree C) for 1, 7, or 28 days. A parallel group was kept at room temperature (unstressed). Unstressed or rats preexposed to 28 days cold were immobilized for 2 hrs and killed by decapitation. The adrenal medullae, separatedly from right and left side, have been dissected and individually frozen at - 70 degree C. We will pool samples from 4 rats per treatment to control for variability.
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Project description:Hormones produced by the adrenal cortex are absolutely essential for numerous processes in living animals. Our research group investigated to what extend the central regulators of deprived oxygen, hypoxia inducible factors (HIFs), contribute to this steroidogenesis. For this, we developed a set of new transgenic mouse lines displaying modified HIF1α and HIF2α levels in cortical cells and revealed that HIF1α exclusively regulates the transcription of a majority of enzymes responsible for the production of glucocorticoids and mineralocorticoids as well as a consequent inflection of cytokines in circulation. These novel tools will be helpful to understand how sustained and chronic changes in adrenocortical hormones can impact during health and disease.
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Project description:MicroRNAs (miRNAs) are small, endogenous, non-protein coding RNAs that are an important means of post-transcriptional gene regulation. Deletion of Dicer, a key miRNA processing enzyme, is embryonic lethal in mice, and tissue-specific Dicer deletion results in developmental defects. Using a conditional knockout model, we generated mice lacking Dicer in the adrenal cortex. These Dicer knockout (KO) mice exhibited perinatal mortality and failure of the adrenal cortex during late gestation between embryonic day 16.5 (E16.5) and E18.5. Further study of Dicer KO adrenals demonstrated a significant loss of Sf1 expressing cortical cells that was histologically evident as early as E16.5 coincident with an increase in p21 and cleaved-caspase 3 staining in the cortex. However, peripheral cortical proliferation persisted in KO adrenals as assessed by anti-PCNA staining. To further characterize the embryonic adrenals from Dicer KO mice, we performed microarray analyses for both gene expression and miRNA on purified RNA isolated from control and KO adrenals of E15.5 and E16.5 embryos. Consistent with the absence of Dicer and the associated loss of miRNA-mediated mRNA degradation, we observed an up-regulation of a small subset of adrenal transcripts in Dicer KO mice, most notably the transcripts coded by the genes Nr6a1 and Acvr1c. Indeed, several miRNAs, including let-7, miR-34c, and miR-21 that are predicted to target these genes for degradation, were also markedly down-regulated in Dicer KO adrenals. Together these data suggest a role for miRNA mediated regulation of a subset of genes that are essential for normal adrenal growth and homeostasis. Adrenals from control and Dicer KO litter mates were pooled separately from 4 individual litters, resulting in a total of 4 control (cre-) and 4 Dicer KO biological replicates at both E15.5 and E16.5.
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