The Stability of the Transcriptome during the Estrous Cycle in Four Regions of the Mouse Brain
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE96700 | GEO | 2017/07/01
SECONDARY ACCESSION(S): PRJNA379422
REPOSITORIES: GEO
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Project description:FecB (also known as BMPR1B) is a crucial gene in sheep reproduction, which has a mutation (A746G) that was found to increase the ovulation rate and litter size. The FecB mutation is associated with reproductive endocrinology, such mutation can control external estrous characteristics and affect follicle-stimulating hormone during the estrous cycle. Previous researches showed that the FecB mutation can regulate the transcriptomic profiles in the reproductive-related tissues including hypothalamus, pituitary, and ovary during the estrous cycle of Small Tailed Han sheep (STH). However, little research has been reported on the correlation between FecB mutation and the estrous cycle in STH sheep oviduct. To investigate the coding and non-coding transcriptomic profiles involved in the estrous cycle and FecB in the sheep oviduct, RNA sequencing was performed to analyze the transcriptomic profiles of mRNAs and long non-coding RNAs (lncRNAs) in the oviduct during the estrous cycle of STH sheep with mutant (FecBBB) and wild-type (FecB++) genotypes. In total, 21,863 lncRNAs and 43,674 mRNAs were screened.Together, our results can provide novel insights into the oviductal transcriptomic function against a FecB mutation background in sheep reproduction.
2023-11-08 | GSE247022 | GEO
Project description:The differentiation of the hormone-producing cell lineages of the anterior pituitary represents an informative model of mammalian cell fate determination. The generation and maintenance of two of these lineages, the growth hormone (GH) producing somatotropes and prolactin (PRL) producing lactotropes, is dependent on the pituitary-specific POU-homeo domain transcription factor, POU1F1. While POU1F1 is expressed in both cell types, and plays a direct and essential role in the activation of both the Gh and Prl genes, GH expression is restricted to somatotropes and PRL expression is restricted to lactotropes. These observations imply the existence of additional, cell type-enriched factors, that contribute to the somatotrope and lactotrope cell identities. Here, we use a set of transgenic mouse models to facilitate sorting of somatotrope and lactotrope populations based on the expression of distinct fluorescent markers expressed under Gh and Prl gene transcriptional controls, respectively. The transcriptomic analyses reveal a concordance of gene expression profiles in the two populations. The limited number of divergent mRNAs between the two populations includes a set of transcription factors that may have roles in pituitary lineage divergence or in regulating the expression of key lineage-specific genes after lineage divergence. Four of these factors were validated for lineage enrichment at the level of protein expression, two somatotrope-enriched and two lactotrope-enriched, and three of these four factors were shown to have corresponding activities in appropriate enhancement or repression of landmark genes. These studies establish a useful database for further study of the somatotrope and lactotrope cells as well as identify novel regulators of lineage marker expression in the anterior pituitary.
2018-10-31 | GSE118863 | GEO
Project description:This a model from the article:
Model-projected mechanistic bases for sex differences in growth hormone
regulation in humans.
Farhy LS, Bowers CY, Veldhuis JD. Am J Physiol Regul Integr Comp Physiol
2007 Apr;292(4):R1577-93 17185408
,
Abstract:
Models of physiological systems facilitate rational experimental design,
inference, and prediction. A recent construct of regulated growth hormone (GH)
secretion interlinks the actions of GH-releasing hormone (GHRH), somatostatin
(SRIF), and GH secretagogues (GHS) with GH feedback in the rat (Farhy LS,
Veldhuis JD. Am J Physiol Regul Integr Comp Physiol 288: R1649-R1663, 2005). In
contrast, no comparable formalism exists to explicate GH dynamics in any other
species. The present analyses explore whether a unifying model structure can
represent species- and sex-defined distinctions in the human and rodent. The
consensus principle that GHRH and GHS synergize in vivo but not in vitro was
explicable by assuming that GHS 1) evokes GHRH release from the brain, 2)
opposes inhibition by SRIF both in the hypothalamus and on the pituitary gland,
and 3) stimulates pituitary GH release directly and additively with GHRH. The
gender-selective principle that GH pulses are larger and more irregular in women
than men was conferrable by way of 4) higher GHRH potency and 5) greater GHS
efficacy. The overall construct predicts GHRH/GHS synergy in the human only in
the presence of SRIF when the brain-pituitary nexus is intact, larger and more
irregular GH pulses in women, and observed gender differences in feedback by GH
and the single and paired actions of GHRH, GHS, and SRIF. The proposed model
platform should enhance the framing and interpretation of novel clinical
hypotheses and create a basis for interspecies generalization of GH-axis
regulation.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Farhy LS, Bowers CY, Veldhuis JD. (2007) - version03
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@aukland.ac.nz
The University of Auckland
The Bioengineering Institute
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 | MODEL0912096133 | BioModels
Project description:Prolactin (Prl) is a pleiotropic hormone with multiple functions in several tissues and organs, including the brain. In the hippocampus, Prl has been implicated in several functions, including neuroprotection against excitotoxicity in lactating rats and in Prl-treated ovariectomized animals. However, the molecular mechanisms involved in Prl actions in the hippocampus have not been completely elucidated. The aim of this study was to analyse the hippocampal transcriptome of female Prl-treated ovariectomized rats. Transcriptomic analysis by RNASeq revealed 162 differentially expressed genes throughout 24 h of Prl treatment. Gene Ontology analysis of those genes showed that 37.65% were involved in brain processes that are regulated by the hippocampus, such as learning, memory and behaviour, as well as new processes that we did not foresee, such as glial differentiation, axogenesis, synaptic transmission, postsynaptic potential, and neuronal and glial migration. Immunodetection analysis demonstrated that Prl significantly modified microglial morphology, reduced the expression of Cd11b/c protein, and altered the content and location of the neuronal proteins Tau, Map2 and Syp, which are involved in axogenic and synaptic functions. This novel delineation of Prl activity in the hippocampus highlights its importance as a neuroactive hormone, opens a new avenue for understanding its actions and supports its participation in neuronal plasticity of this brain area.
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Project description:Brain structure and function are sexually dimorphic. As neuroscience research has largely focused on the male brain and behavior, the female brain and, in particular, its inherent dynamics have been left underexplored. During the mammalian reproductive period, the female brain is exposed to fluctuating hormone levels over the cycles known as menstrual (in humans) or estrous (in rodents). Variation in estradiol levels has been shown to affect synaptic plasticity in the female brain, including changes in dendritic spine density systematically across the estrous cycle. Female emotionality and cognitive function vary with physiologically fluctuating sex hormone levels. However, the molecular mechanisms underlying the dynamic nature of the female brain structure and function are currently unknown. Here we show that neuronal chromatin organization in the female ventral hippocampus of mouse is dynamic and fluctuates across the estrous cycle. We find changes in chromatin organization associated with the transcriptional activity of nearby genes important for neuronal function, neurotransmission, synapse formation, and behavior. We also link these chromatin dynamics to variation in anxiety-like behavior and to fluctuations in dendritic spine and synaptic density in the ventral hippocampus. In terms of chromatin structure, within-female and between-sex variation are of similar magnitudes, emphasizing the importance of accounting for fluctuating sex-hormone levels in females in the studies of the brain epigenome and behavior. These results provide critical insights into the mechanisms underlying sex-hormone and sex-dependent variation in adult brain structure and function. The study also has implications for better understanding of sex-biased disorders such as depression and anxiety which are strongly associated with sex-hormone status in females and are twice as prevalent in women than in men. This study establishes a foundation for the development of sex-specific approaches to treat sex-biased neuropsychiatric disorders including depression and anxiety disorders.
2019-05-03 | GSE114036 | GEO
Project description:The knowledge regarding the reproductive-status-related changes occurring within the transcriptome of the porcine pituitary is limited. This study aimed to compare pituitary gland gene expression profiles of pigs during the maternal recognition of pregnancy period (days 12-13 of pregnancy) with pigs during the respective days of the estrous cycle using a microarray approach. Analysis indicated 482 differentially expressed genes (DEGs) with a FC ≥ 1.5 (p < 0.05) in the pituitary of pregnant vs. estrous-cyclic pigs. Among them, 68 were up-regulated and 414 were down-regulated. The evaluated DEGs were annotated to 39 gene ontology (GO) biological processes terms, 13 GO cellular components terms, and 10 GO molecular function terms. Among the evaluated DEGs were selected genes coding for proteins potentially involved in the regulation of early pregnancy in pigs and used for gene interaction analysis and validation of microarray results. Analysis of the relationships among DEGs during maternal recognition of pregnancy showed that some of them are connected with, i.e., TGFβ signaling pathway, follicle-stimulating hormone, prolactin, and growth hormone synthesis or activity, adipocytokines responsivity, angiogenesis, immune response, prostaglandin synthesis and inter-pituitary cell to cell interactions. The findings expand the knowledge regarding the molecular mechanisms appearing in the pituitary in pigs during the maternal recognition period of pregnancy.
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Project description:This study, using a growth hormone (GH)-deficient dwarf animal model and peripheral GH replacement, investigated the effects of circulating IGF-1 during adolescence on IGF-1 levels in the brain. Our results demonstrated that hippocampal IGF-1 protein concentrations during adolescence are highly regulated by circulating IGF-1, which were reduced by GH deficiency and restored by systematic GH replacement. In contrast, IGF-1 levels in the CSF were decreased by GH deficiency but not restored by GH replacement. Furthermore, analysis of gene expression using microarrays and RT-PCR indicated that circulating IGF-1 levels did not modify the transcription of IGF-1 or its receptor in the hippocampus but did regulate genes that are involved in microvascular structure and function, brain development, and synaptic plasticity, which potentially support brain structures involved in cognitive function during this important developmental period.
2011-07-21 | GSE29512 | GEO
Project description:The developmental transition to motherhood requires gene expression changes that alter the brain to prepare and drive the female to perform maternal behaviors. Furthermore, it is expected that the many physiological changes accompanying pregnancy and postpartum stages will impact brain gene expression patterns. To understand how extensive these gene expression changes are, we examined the global transcriptional response broadly, by examining four different brain regions: hypothalamus, hippocampus, neocortex, and cerebellum. Further, to understand the time course of these changes we performed RNA-sequencing analyses on mRNA derived from virgin females, two pregnancy time points and three postpartum time points. We find that each brain region and time point shows a unique molecular signature, with only 49 genes differentially expressed in all four regions, across the time points. Additionally, several genes previously implicated in underlying postpartum depression change expression. This study serves as a comprehensive atlas of gene expression changes in the maternal brain in the cerebellum, hippocampus, hypothalamus, and neocortex. At each of the time points analyzed, all four brain regions show extensive changes, suggesting that pregnancy, parturition, and postpartum maternal experience substantially impacts diverse brain regions. Libraries were prepared from three independent biological replicates, mRNA for each biological replicate was derived from a single mouse brain, with each mouse brain being used to collect all four brain regions.
2016-07-03 | E-GEOD-70732 | biostudies-arrayexpress
Project description:This study, using a growth hormone (GH)-deficient dwarf animal model and peripheral GH replacement, investigated the effects of circulating IGF-1 during adolescence on IGF-1 levels in the brain. Our results demonstrated that hippocampal IGF-1 protein concentrations during adolescence are highly regulated by circulating IGF-1, which were reduced by GH deficiency and restored by systematic GH replacement. In contrast, IGF-1 levels in the CSF were decreased by GH deficiency but not restored by GH replacement. Furthermore, analysis of gene expression using microarrays and RT-PCR indicated that circulating IGF-1 levels did not modify the transcription of IGF-1 or its receptor in the hippocampus but did regulate genes that are involved in microvascular structure and function, brain development, and synaptic plasticity, which potentially support brain structures involved in cognitive function during this important developmental period. GH-deficient dwarf (dw/dw) and heterozygous (HZ) rats were identified at postnatal day 33-34. Starting from d35, dw/dw rats received subcutaneous injection of either 300µg GH (dw/dw+GH) or saline (dw/dw+sal) for 7d or 30d. HZ animals received saline for the same periods as controls. Animals (n=4/group for each time point) were sacrificed, the hippocampi were dissected, and total RNA were isolated for subsequent transcriptomic profiling.
2011-07-20 | E-GEOD-29512 | biostudies-arrayexpress
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