Effect of depletion of GPR30 on gene expression in female C57BL/6J mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE212893 | GEO | 2023/08/10
REPOSITORIES: GEO
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Project description:G-1 is an agonist to GPR30. Activation of GPR30 by G-1 inhibited prostate cancer cell growth in LNCaP xenografts regrown after catration of the host (nude mice), but not in the androgen-sensitive LNCaP xenograft grown in an intact host. Results provide insights into the molecular basis of G-1 action in castration-resistant prostate cancer.
2014-02-14 | GSE54974 | GEO
Project description:Although the methylation status of histone H3K27 plays a critical role in CD4+ T cell differentiation and its function, the role of Utx, histone H3K27 demethylase, in the CD8+ T cell-dependent immune response remains unclear. We therefore generated T cell-specific Utx knockout (Utx KO) mice to determine the role of Utx in CD8+ T cells. Wild-type (WT) and Utx KO mice were infected with Listeria monocytogenes expressing OVA to analyze the immune response of Ag-specific CD8+ T cells upon primary and secondary infections. There was no significant differences in the primary expansion of Ag-specific CD8+ T cells between WT and Utx KO mice. However, Utx deficiency resulted in an increased secondary expansion of Ag-specific CD8+ T cells. Adoptive transferred Utx KO CD8+ T cells resulted in increased numbers of CD127hi KLRG1lo memory precursors in the primary expansion and larger numbers of memory cells. We observed a decreased gene expression of effector-associated transcription factors, including Prdm1 encoding Blimp1, in Utx KO CD8+ T cells upon primary infection. We confirmed that the tri-methylation level of histone H3K27 in the Prdm1 gene loci in the Utx KO cells was higher than in the WT cells. The treatment of CD8+ T cells with Utx-cofactor α-ketoglutarate hampered the memory formation, while Utx-inhibitor GSK-J4 enhanced the memory formation and increased the secondary expansion in WT CD8+ T cells. These data suggest that Utx negatively controls the memory formation of Ag-stimulated CD8+ T cells by epigenetically regulating the expression of genes, including Prdm1. Based on these findings, we identified a critical link between Utx and the differentiation of Ag-stimulated CD8+ T cells upon infection
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Project description:The physical manifestations of memory formation and recall are fundamental questions that remain unresolved. At the cellular level, ensembles of neurons called engrams are activated by learning events and control memory recall. Astrocytes are in close proximity to neurons and engage in a range of activities that support neurotransmission and circuit plasticity. Moreover, astrocytes exhibit experience dependent plasticity; however whether specific ensembles of astrocytes participate in memory recall remains obscure. Here we show that learning events induce c-Fos expression in a subset of hippocampal astrocytes, which subsequently regulates hippocampal circuit function. Intersectional, c-Fos based labeling of these astrocyte ensembles after learning events reveals that they are closely affiliated with engram neurons, while re-activation of these astrocyte ensembles stimulates memory recall. At the molecular level, these astrocyte ensembles exhibit elevated expression of NFIA and its selective deletion from this population suppresses memory recall. Together, our studies identify learning-associated astrocyte ensembles as a new form of plasticity that is sufficient to provoke memory recall, while implicating astrocytes as a reservoir for the storage of memories.
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Project description:Gene expression analyses were carried out to identify genes regulated by 17-beta estradiol (E2) and Hydroxytamoxifen (OHT) through GPR30 in SKBR3 cells, a breast cancer cell-line which expresses GPR30 but lacks Estrogen Receptor alpha or beta. Keywords: Gene expression analysis, Non-genomic signaling in breast cancer cells.
2009-02-19 | GSE11567 | GEO
Project description:G-1 is an agonist to GPR30. Activation of GPR30 by G-1 inhibited prostate cancer cell growth in LNCaP xenografts regrown after catration of the host (nude mice), but not in the androgen-sensitive LNCaP xenograft grown in an intact host. Results provide insights into the molecular basis of G-1 action in castration-resistant prostate cancer. Male nude mice were injected with LNCaP cells. When the LNCaP tumors reached 150–300 mm3, mice were divided into two groups: intact (androgen-sensitive tumor) and castrated. For the intact group, mice were subcutaneously injected with vehicle alone (95% PBS, 2.5% DMSO, 2.5% ethanol) or G-1 (4 mg/kg/day in vehicle) daily for 16 days. For the castrated group, tumors regressed and then regrew to ~300-400mm3. Mice were treated daily with vehicle or G-1 as described for 16 days. Tumors were harvested for RNA extraction and microarray experiments.
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Project description:Gene expression analyses were carried out to identify genes regulated by 17-beta estradiol (E2) and Hydroxytamoxifen (OHT) through GPR30 in SKBR3 cells, a breast cancer cell-line which expresses GPR30 but lacks Estrogen Receptor alpha or beta. Keywords: Gene expression analysis, Non-genomic signaling in breast cancer cells. Gene expression analyses were done for control transfected SKBR3 cells: 1) Uninduced, 2) Induced with 10 microM OHT, 3) Induced with 1 microM E2 and 4) GPR30-antisense transfected cells induced with 10 microM OHT. The cells were induced for 1h and all the samples were collected in triplicates.
2009-02-19 | E-GEOD-11567 | biostudies-arrayexpress
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Project description:CRTC3 is CREB regulated transcriptional co-activators and prominently expressed in astrocyte cells. CRTC3 plays a specific role in determining the social heirarchical ranking in mice by confirming social rank test in CRTC3 KO mice. Loss of CRTC3 in astrocyte induced neuronal change and caused exchanging protein expression pattern. We used microarrays to determine the astrocyte-derived factors that were regulated by CRTC3 and related with social dominance behaviours of CRTC3 KO mice. We identifed distinct factor of down-regulated gene during primary astrocyte cell in CRTC3 KO.
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Project description:Among all voltage-gated calcium channels, the T-type Ca2+ channels encoded by the Cav3 genes are highly expressed in the hippocampus, which is associated with contextual, temporal and spatial learning and memory. However, the specific involvement of the Cav3.2 T-type Ca2+ channel in these hippocampus-dependent types of learning and memory remains unclear. To investigate the functional role of the 1H channel in learning and memory, we subjected Cav3.2 homozygous, heterozygous knockout and their wild-type littermates to hippocampus-dependent behavioral tasks, including trace fear conditioning (TFC), the Morris water-maze and passive avoidance. The Cav3.2-/- mice performed normally in the Morris water-maze and auditory trace fear conditioning tasks but were impaired in the context-cued trace fear conditioning, step-down and step-through passive avoidance tasks. Furthermore, long-term potentiation (LTP) could be induced for 180 minutes in hippocampal slices of WTs and Cav3.2+/- mice, whereas LTP persisted for only 120 minutes in Cav3.2-/- mice. To determine whether the hippocampal formation is responsible for the impaired behavioral phenotypes , we next performed experiments locally knock down function of the Cav3.2 T-type Ca2+ channel in the hippocampus. Wild-type mice infused with mibefradil exhibited similar behaviors as homozygous knockouts. Finally, microarray analyses indicated that Cav3.2-/- and WT mice presented distinct hippocampal transcriptome profiles. Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Cav3.2 T-type Ca2+ channel. After WT and Cav3.2 KO mice retrieval of context-associated memory, three right hippocampi of each group were dissected, pooled together and homogenized. The products of experimental and naive groups were used to acquire expression profiles of a total of 29,922 unique genes. Two replicates per group.
2013-02-28 | E-GEOD-30845 | biostudies-arrayexpress
Project description:Among all voltage-gated calcium channels, the T-type Ca2+ channels encoded by the Cav3 genes are highly expressed in the hippocampus, which is associated with contextual, temporal and spatial learning and memory. However, the specific involvement of the Cav3.2 T-type Ca2+ channel in these hippocampus-dependent types of learning and memory remains unclear. To investigate the functional role of the 1H channel in learning and memory, we subjected Cav3.2 homozygous, heterozygous knockout and their wild-type littermates to hippocampus-dependent behavioral tasks, including trace fear conditioning (TFC), the Morris water-maze and passive avoidance. The Cav3.2-/- mice performed normally in the Morris water-maze and auditory trace fear conditioning tasks but were impaired in the context-cued trace fear conditioning, step-down and step-through passive avoidance tasks. Furthermore, long-term potentiation (LTP) could be induced for 180 minutes in hippocampal slices of WTs and Cav3.2+/- mice, whereas LTP persisted for only 120 minutes in Cav3.2-/- mice. To determine whether the hippocampal formation is responsible for the impaired behavioral phenotypes , we next performed experiments locally knock down function of the Cav3.2 T-type Ca2+ channel in the hippocampus. Wild-type mice infused with mibefradil exhibited similar behaviors as homozygous knockouts. Finally, microarray analyses indicated that Cav3.2-/- and WT mice presented distinct hippocampal transcriptome profiles. Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Cav3.2 T-type Ca2+ channel. After WT and Cav3.2 KO mice retrieval of context-associated memory, three left hippocampi of each group were dissected, pooled together and homogenized. The products of experimental and naive groups were used to acquire expression profiles of a total of 29,922 unique genes. Two replicates per group.
2013-02-28 | E-GEOD-30842 | biostudies-arrayexpress