Reactivity of the corticotrope axis in rainbow trout (Oncorhynchus mykiss) exposed to chronic environmental stress
Ontology highlight
ABSTRACT:
ORGANISM(S): Oncorhynchus mykiss
PROVIDER: GSE126748 | GEO | 2021/02/01
REPOSITORIES: GEO
Similar Datasets
Project description:Purpose: Offspring from females that experience stressful conditions during reproduction often exhibit altered phenotypes and many of these effects are thought to arise due to increased exposure to maternal glucocorticoids. Here we used RNAseq to test whether the embryonic transcriptional response to increased levels of cortisol was similar to the transcriptional response to maternal stress in sticklebacks Methods: Eggs were treated by immersing eggs for 30 mins in water that contained 0, 5, or 10 ug/L, which represented baseline, predator induced, and super physiological levels of maternally derived cortisol. To isolated enough RNA for RNAseq, 10 embyros from each clutch/treatment were pooled prior to RNA extraction for a total of 18 pools (6 clutches x 3 treatments). Results: Analysis of genome-wide transcriptional profiles suggests that 17251 (genes which survived a cut-off of having cpm more than 1 in at least two samples; and had a significant likelihood ratio calculated in edgeR) genes out of the possible 22,456 genes in the stickleback genome were expressed in 72-hour embryos. However, we did not detect any differences in gene expression between embryos that were treated with cortisol compared to the control group. mRNA profiles of egg clutches treated with 0, 5, or 10 ug/L are compared, which represented baseline, predator induced, and super physiological levels of maternally derived cortisol.
2015-08-03 | E-GEOD-71649 | biostudies-arrayexpress
Project description:Purpose: Offspring from females that experience stressful conditions during reproduction often exhibit altered phenotypes and many of these effects are thought to arise due to increased exposure to maternal glucocorticoids. Here we used RNAseq to test whether the embryonic transcriptional response to increased levels of cortisol was similar to the transcriptional response to maternal stress in sticklebacks Methods: Eggs were treated by immersing eggs for 30 mins in water that contained 0, 5, or 10 ug/L, which represented baseline, predator induced, and super physiological levels of maternally derived cortisol. To isolated enough RNA for RNAseq, 10 embyros from each clutch/treatment were pooled prior to RNA extraction for a total of 18 pools (6 clutches x 3 treatments). Results: Analysis of genome-wide transcriptional profiles suggests that 17251 (genes which survived a cut-off of having cpm more than 1 in at least two samples; and had a significant likelihood ratio calculated in edgeR) genes out of the possible 22,456 genes in the stickleback genome were expressed in 72-hour embryos. However, we did not detect any differences in gene expression between embryos that were treated with cortisol compared to the control group.
2015-08-03 | GSE71649 | GEO
Project description:Major Depression (MDD) is a prevalent psychiatric disorder and exposure to stress is robust risk factor for MDD. Clinical data and rodent models have indicated the negative impact of chronic stress induced hormones like cortisol on brain volume, memory, and cell metabolism. However, the cellular and transcriptomic changes that occur in the brain after prolonged exposure to cortisol are less understood. Furthermore, astrocyte-specific contribution to cortisol-induced neuropathology remains understudied. Here, we have developed an in vitro model of “chronic stress” using human induced pluripotent stem cell-derived astrocytes treated with cortisol for 7 days. Whole transcriptome sequencing reveals differentially expressed genes (DEGs) uniquely regulated in chronic cortisol compared to acute cortisol treatment. Utilizing this paradigm, we examined the stress response transcriptome of astrocytes generated from MDD patient iPSCs. MDD-specific DEGs related to GPCR ligand binding, synaptic signaling, and ion homeostasis. Together, these data highlight the unique role astrocytes play in the central nervous system and present interesting genes for future study into the relationship between chronic stress and MDD.
2022-10-04 | GSE178071 | GEO
Project description:This a model from the article:
Inclusion of the glucocorticoid receptor in a hypothalamic pituitary adrenal
axis model reveals bistability.
Gupta S, Aslakson E, Gurbaxani BM, Vernon SD. Theor Biol Med Model
2007 Feb 14;4:8 17300722
,
Abstract:
BACKGROUND: The body's primary stress management system is the hypothalamic
pituitary adrenal (HPA) axis. The HPA axis responds to physical and mental
challenge to maintain homeostasis in part by controlling the body's cortisol
level. Dysregulation of the HPA axis is implicated in numerous stress-related
diseases. RESULTS: We developed a structured model of the HPA axis that includes
the glucocorticoid receptor (GR). This model incorporates nonlinear kinetics of
pituitary GR synthesis. The nonlinear effect arises from the fact that GR
homodimerizes after cortisol activation and induces its own synthesis in the
pituitary. This homodimerization makes possible two stable steady states (low
and high) and one unstable state of cortisol production resulting in bistability
of the HPA axis. In this model, low GR concentration represents the normal
steady state, and high GR concentration represents a dysregulated steady state.
A short stress in the normal steady state produces a small perturbation in the
GR concentration that quickly returns to normal levels. Long, repeated stress
produces persistent and high GR concentration that does not return to baseline
forcing the HPA axis to an alternate steady state. One consequence of increased
steady state GR is reduced steady state cortisol, which has been observed in
some stress related disorders such as Chronic Fatigue Syndrome (CFS).
CONCLUSION: Inclusion of pituitary GR expression resulted in a biologically
plausible model of HPA axis bistability and hypocortisolism. High GR
concentration enhanced cortisol negative feedback on the hypothalamus and forced
the HPA axis into an alternative, low cortisol state. This model can be used to
explore mechanisms underlying disorders of the HPA axis.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Gupta S, Aslakson E, Gurbaxani BM, Vernon SD. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230036 | BioModels
Project description:This a model from the article:
Inclusion of the glucocorticoid receptor in a hypothalamic pituitary adrenal
axis model reveals bistability.
Gupta S, Aslakson E, Gurbaxani BM, Vernon SD. Theor Biol Med Model
2007 Feb 14;4:8 17300722
,
Abstract:
BACKGROUND: The body's primary stress management system is the hypothalamic
pituitary adrenal (HPA) axis. The HPA axis responds to physical and mental
challenge to maintain homeostasis in part by controlling the body's cortisol
level. Dysregulation of the HPA axis is implicated in numerous stress-related
diseases. RESULTS: We developed a structured model of the HPA axis that includes
the glucocorticoid receptor (GR). This model incorporates nonlinear kinetics of
pituitary GR synthesis. The nonlinear effect arises from the fact that GR
homodimerizes after cortisol activation and induces its own synthesis in the
pituitary. This homodimerization makes possible two stable steady states (low
and high) and one unstable state of cortisol production resulting in bistability
of the HPA axis. In this model, low GR concentration represents the normal
steady state, and high GR concentration represents a dysregulated steady state.
A short stress in the normal steady state produces a small perturbation in the
GR concentration that quickly returns to normal levels. Long, repeated stress
produces persistent and high GR concentration that does not return to baseline
forcing the HPA axis to an alternate steady state. One consequence of increased
steady state GR is reduced steady state cortisol, which has been observed in
some stress related disorders such as Chronic Fatigue Syndrome (CFS).
CONCLUSION: Inclusion of pituitary GR expression resulted in a biologically
plausible model of HPA axis bistability and hypocortisolism. High GR
concentration enhanced cortisol negative feedback on the hypothalamus and forced
the HPA axis into an alternative, low cortisol state. This model can be used to
explore mechanisms underlying disorders of the HPA axis.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Gupta S, Aslakson E, Gurbaxani BM, Vernon SD. (2007) - version=1.0
The original CellML model was created by:
Catherine Lloyd
c.lloyd@auckland.ac.nz
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL1006230111 | BioModels
Project description:This a model from the article:
A computer simulation of the hypothalamic-pituitary-adrenal axis.
Gonzalez-Heydrich J, Steingard RJ, Kohane I. Proc Annu Symp Comput Appl Med Care
1994;:1010 7949852
,
Abstract:
This paper describes the construction of a computer model that simulates the
hypothalamic-pituitary-adrenal axis (HPA axis) regulation of cortisol
production. It is presented to illustrate the process of physiological modeling
using standard "off the shelf" technologies. The model simulates components of
the HPA axis involved in the continuous secretion and elimination of cortisol,
adrenocorticotropin (ACTH), and corticotropin releasing hormone (CRH). The
physiological relations of these component pieces were modeled based on the
current knowledge of their functioning. Rate constants, half lives, and receptor
affinities were assigned values derived from the experimental literature. At its
current level of development the model is able to accurately simulate the
timing, magnitude and decay of the ACTH and cortisol concentration peaks
resulting from the ovine-CRH stimulation test in normal and hypercortisolemic
patients. The model will be used to predict the effects of lesions in different
components of the HPA axis on the time course of cortisol and ACTH levels. We
plan to use the model to explore the experimental conditions required to
distinguish mechanisms underlying various disorders of the HPA axis,
particularly depression. Efforts are currently underway to validate the model
for a large variety of normal and pathological perturbations of the HPA axis.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Gonzalez-Heydrich J, Steingard RJ, Kohane I. (1994) - version02
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
2005-01-01 | MODEL0911270004 | BioModels
Project description:Water and ToxB-infiltrated leaves of sensitive cultivar Katepwa were collected at 0,3,9,14,24,48 hours post infiltration (hpi), total RNA was extracted and processed. Expression levels were obtained using Affymetrix GeneChip Wheat Genome Array
2012-09-01 | E-MTAB-963 | biostudies-arrayexpress
Project description:Exposure to serious or traumatic events early in life can lead to persistent alterations in physiological stress response systems, including enhanced cross-talk between the neuroendocrine and immune system. These programming effects may be mechanistically involved in mediating the effects of adverse childhood experience on disease risk in adulthood. Here, we investigated neuroendocrine as well as genome-wide mRNA expression responses in monocytes to acute stress exposure, in a sample of healthy adults (n=30) with a history of early childhood adversity, and a control group (n=30) without trauma experience. The early adversity group showed altered hypothalamus-pituitary-adrenal (HPA) axis responses to stress, evidenced by lower ACTH and cortisol responses. Analyses of gene expression patterns showed a larger stress-induced increase of cardinal pro-inflammatory transcripts IL6 and FOSB, and an increased activity of pro-inflammatory upstream signaling in the early adversity group. We also identified transcripts that were differentially correlated with stress-induced cortisol increases between the groups. Noteworthy, FKBP5 expression was less responsive to cortisol induction in the early adversity group, with potential effects on the ultra-short feedback loop that balances FKBP5 and glucocorticoid receptor activity. Further exploratory analyses showed differential stress-induced regulation of gene transcription between the groups. Prominent among the differentially regulated transcripts were those coding for genes involved in signal transducer activity, G-protein coupled receptors, and several genes involved in serotonin receptor signaling. We suggest that childhood adversity leads to persistent alterations in transcriptional control of stress responsive pathways, which - when chronically or repeatedly activated - might predispose individuals to stress-related psychopathology.
2015-11-30 | GSE70603 | GEO
Project description:The purpose of this study was to develop a comprehensive picture of the host transcriptional response during the acute stage of melioidosis. To adress this, we compared the transcriptome of infected liver and spleen with uninfected tissues over an infection period of 42 hr (16 hpi, 24 hpi and 42 hpi, respectively) to identify genes whose expression is altered in response to an acute infection.
2010-12-23 | GSE25074 | GEO
Project description:Limited studies on neurotoxicity following chronic exposure to butyl-paraben (BuP) have been conducted. In this study, neurobehavior in zebrafish adults was assessed using a novel tank test, photomotor response tests, and T-maze tests after exposure to BuP for 28 days at the concentrations of 0, 0.01, 0.1, and 1.0 mg/L. To comprehensively understand the underlying molecular perturbations in the brain, alterations in transcripts, neurotransmitters, and neurosteroids were measured. We found that BuP penetrated the blood-brain barrier and impaired neurobehavior in photosensitivity at 1.0 mg/L and in memory at 0.1 and 1.0 mg/L. RNA-seq analysis showed that phototransduction, tight junctions, and neuroactive ligand receptor activity were significantly affected, which explains the observed abnormal neurobehaviors. Neurosteroid analysis revealed that BuP increased cortisol levels in a concentration-dependent manner and specifically reduced allopregnanolone levels at all tested concentrations, suggesting that cortisol and allopregnanolone are significant neurosteroid markers associated with photosensitivity and memory deficits. Collectively, we demonstrated that BuP can cross the blood-brain and modulates the levels of transcripts, associated with phototransduction and circadian rhythm, and neurosteroidal cortisol and allopregnanolone, resulting in abnormal neurobehavioral responses to light stimulation and learning and memory.
2022-08-21 | GSE211530 | GEO