ChIP-chip from pregnant female mouse pituitary with POU1F1 (PIT-1)
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE33318 | GEO | 2011/10/29
SECONDARY ACCESSION(S): PRJNA149305
REPOSITORIES: GEO
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Project description:POU1F1 regulates, in the pituitary, the development of the prolactin-, growth hormone- and thyrotropin ß-expressing lineages and the expression of these hormone in the mature pituitary through the direct regulation of their promoters. Besides these functions, POU1F1 is also involved in other cellular processes in the pituitary, such as cell division and survival, but the genomic targets involved in these actions are not known. The present ChIP-chip study identified a large number of hitherto unknown potential direct targets that might be involved in these actions, such as Tcf4, Lmo4, Pax6, Trp53 etc. ChIP-chip was done from pregnant female mouse (C57Bl/6J) pituitary (3 pools of 12 pituitary anterior lobes, corresponding to three biological replicates) with POU1F1 (PIT-1)
2011-10-28 | E-GEOD-33318 | biostudies-arrayexpress
Project description:Prolactin (PRL) is an important hormone that is secreted by the pituitary gland and plays an important role in the growth, development and reproduction of organisms. Thyrotropin-releasing hormone (TRH) is a common prolactin-releasing factor that regulates the synthesis and secretion of prolactin. In recent studies, microRNAs (miRNAs) have been found to play a key role in the regulation of pituitary hormones. However, there is a lack of systematic studies on the regulatory role that TRH plays on the pituitary transcriptome, and the role of miRNAs in the regulation of PRL synthesis and secretion by TRH lacks experimental evidence. In this study, we first investigated the changes in PRL synthesis and secretion in the rat pituitary gland after TRH administration. The results of transcriptomic analysis after TRH treatment showed that 102 genes, including those that encode Nppc, Fgf1, PRL, Cd63, Npw, and Il23a, were upregulated, and 488 genes, including those that encode Lats1, Cacna2d1, Top2a, and Tfap2a, were downregulated. These genes are all involved in the regulation of prolactin expression. The gene expression of miR-126a-5p, which regulates the level of PRL in the pituitary gland, was screened by analysis prediction software and by a dual luciferase reporter system. The data presented in this study demonstrate that TRH can regulate prolactin synthesis and secretion through miR-126a-5p, thereby improving our understanding of the molecular mechanism of TRH-mediated PRL secretion and providing a theoretical basis for the role of miRNAs in regulating the secretion of pituitary hormones.
2024-06-01 | GSE221560 | 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:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed maternal production of prolactin, a pituitary hormone essential for nursing including milk production, during the lactational stage. To comprehensively investigate genes linked to the lower prolactin expression, we performed a DNA microarray analysis in the hypothalamus, which regulates the pituitary prolactin synthesis, of lactating dam rats.
2020-06-19 | GSE135931 | GEO
Project description:The aim of the study is to evaluate Pit-1-induced genes in the MCF-7 cell line The Pit-1 transcription factor (also known as POU1F1) plays a critical role in cell differentiation during organogenesis of the anterior pituitary in mammals and is a transcriptional activator for pituitary gene transcription. Increased expression of Pit-1 has been reported in human tumorigenic breast cells. Here, we found that Pit-1 overexpression or knockdown in human breast cancer cell lines induced profound phenotypic changes in the expression of proteins involved in cell proliferation, apoptosis, and invasion. In immunodeficient mice, Pit-1 overexpression induced tumoral growth and promoted metastasis in lung. In patients with invasive ductal carcinoma of the breast and node-positive tumors elevated expression of Pit-1 was significantly and independently associated with the occurrence of distant metastasis. These findings suggest that Pit-1 could help to make a more accurate prognosis in patients with node positive breast cancer and may represent a new therapeutic target (Journal of Clinical Investigation 2010, 120:4289-4302)
2014-12-12 | GSE64101 | GEO
Project description:We found that oral administration of TCDD (1 µg/kg) to pregnant rats on gestational day 15 suppressed maternal production of prolactin, a pituitary hormone essential for nursing including milk production, during the lactational stage. To comprehensively investigate genes linked to the lower prolactin expression, we performed a DNA microarray analysis in the pituitary of lactating dam rats.
2020-06-19 | GSE135932 | GEO
Project description:The purpose of this research is to determine whether the drug, Bevacizumab (a monoclonal anti VEGF-A antibody), which is approved to treat patients with metastatic colon cancer induces hyperprolactinemia (increased prolactin secretion) in humans with intact pituitary function. Past studies have shown Bevacizumab to shrink tumor size and also increase prolactin levels. The mechanism of the hyperprolactinemia might be inhibition of pituitary portal vein transport, suggesting that Bevacizumab induces prolactin secretion from normal lactotrophs in the pituitary gland.
Patients who have been treated with Bevacizumab for at least one month will be recruited to participate.
The subjects who are being treated with Bevacizumab by Dr. Stephen Wolin (a sub-investigator) will be screened by him for study eligibility. Dr. Wolin will approach eligible patients with all the information and background of the study and see if they have an interest in being consented.
If consented, there will be 2 blood draws for the research that is not part of their standard care in which 10 ml of blood is collected and prolactin, growth hormone, IGF-I, TSH, thyroxine, ACTH, and cortisol will be measured. One 5ml blood draw will occur before the administration of Bevacizumab and the second 5 ml blood draw will occur after the administration of the Bevacizumab. The investigators will then review the laboratory results. The blood tests are of the hormones of the pituitary gland to test pituitary function and see if there are any abnormalities with the secretions of the gland. Pituitary function abnormalities and hyperprolactinemia are diagnosed by looking at hormone levels in the blood and comparing them to the normal reference ranges.
This study will only involve 10 subjects and will be conducted entirely at Cedars-Sinai Medical Center.
| 2077752 | ecrin-mdr-crc
Project description:The aim of the study is to evaluate Pit-1-induced genes in the MCF-7 cell line The Pit-1 transcription factor (also known as POU1F1) plays a critical role in cell differentiation during organogenesis of the anterior pituitary in mammals and is a transcriptional activator for pituitary gene transcription. Increased expression of Pit-1 has been reported in human tumorigenic breast cells. Here, we found that Pit-1 overexpression or knockdown in human breast cancer cell lines induced profound phenotypic changes in the expression of proteins involved in cell proliferation, apoptosis, and invasion. In immunodeficient mice, Pit-1 overexpression induced tumoral growth and promoted metastasis in lung. In patients with invasive ductal carcinoma of the breast and node-positive tumors elevated expression of Pit-1 was significantly and independently associated with the occurrence of distant metastasis. These findings suggest that Pit-1 could help to make a more accurate prognosis in patients with node positive breast cancer and may represent a new therapeutic target (Journal of Clinical Investigation 2010, 120:4289-4302) MCF-7 cells were transfected with the pcDNA3 (control, two samples as condition, named C1 and C2) or the pcDNA3-Pit-1 overexpression vector (two samples as condition, named 1+ and 2+) for 48 hours.
2014-12-12 | E-GEOD-64101 | biostudies-arrayexpress
Project description:Pituitary gland function is regulated by the activity of various transcription factors which control cell fate decisions leading to cellular differentiation and hormone production. FOXO1 is necessary for the proper timing of somatotrope differentiation and for somatotrope function, but the exact mechanism of action has yet to be elucidated. Recent data implicate FOXO1 in the regulation of genes important for somatotrope differentiation including Gh1, Neurod4, and Pou1f1. Previously, a mouse model with conditional deletion of Foxo1 from the developing pituitary gland displayed reduced Gh1 and Neurod4 transcripts as early as embryonic day 18.5. Additional data from adult animals with conditional deletion of both Foxo1 and Foxo3 from the pituitary gland have a similar reduction in Neurod4 and Gh1, as well as Pou1f1. To investigate the mechanism by which FOXO1 regulates pituitary gland gene expression and confirm in vivo findings, the somatotrope-like cell line, GH3, was treated with the FOXO1 inhibitor, AS1842856, for 24 hours at various concentrations. Neurod4 was the most severely affected genes with a dose-dependent reduction in transcript at inhibitor concentrations as low as 30 nM. Gh1 transcripts were significantly reduced at 300 nM. Pou1f1 expression was trending down at 3 microM inhibitor (p=0.066). Consistent with these findings, CRISPR/Cas9-mediated deletion of Foxo1 in GH3 cells significantly reduced expression of Gh1, Neurod4, but not Pou1f1. To elucidate the molecular mechanisms underlying the role of FOXO1 in somatotropes, ChIPseq was performed for FOXO1 in the GH3 cell line. This study identified novel FOXO1 binding sites associated with the Neurod4, Gh1, and Pou1f1 genes. The FOXO1 binding site in the Neurod4 gene exhibits enhancer activity in somatotrope-like cells, but not in gonadotrope-like or heterologous cells. These data strongly suggest FOXO1 directly contributes to the transcriptional control of genes important for somatotrope differentiation. These novel findings contribute to the much-needed understanding of pituitary cell fate decisions.
2023-12-14 | GSE245740 | GEO
Project description:The high energetic cost of reproduction requires that female fertility be closely linked to metabolic status. However, the mechanisms by which the metabolic and reproductive systems communicate is still largely undefined. We have previously reported that signaling through the major metabolic cytokine leptin controls levels of the pituitary maturation determinant POU1F1 (also referred to as Pit1) that is required for optimal reproductive function. These studies further indicated that leptin increases POU1F1levels in females by promoting Pou1f1 mRNA translation, although the mechanism ofPou1f1 mRNA translation control is unknown. In this study, we report that the stem cell marker and mRNA translational control protein, Musashi, represses translation of the Pou1f1 mRNA. In FACS-sorted purified female somatotropes, Msi1 mRNA and Musashi protein levels are increased in the mouse model that lacks leptin signaling (Gh-CRE leprLepr-null), coincident with the observed attenuation of Pou1f1 mRNA translation. Single-cell RNA sequencing of pituitary cells from control female animals indicates that Msi1 and Pou1f1 mRNAs are co-expressed in Gh-expressing cells and immunocytochemistry analyses of these cells confirms that Musashi protein is present in the GH-containing somatotrope population. We demonstrate that Musashi interacts directly with the Pou1f1 mRNA 3’ UTR and exerts translational repression of a Pou1f1 mRNA translation reporter in vitro, and interacts with the Pou1f1 mRNA in vivo. These findings indicate a critical role for Musashi-mediated mRNA translational regulation in the coordination between metabolic status and the maturation of pituitary somatotropes that is required for optimized reproductive function .
2021-01-11 | GSE153045 | GEO