RNA-sequencing of SVF-derived preadipocytes and adipocytes from inguinal white adipose tissue of male mice treated with vehicle, CGRPa, NPY, NE, or SP
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE293584 | GEO | 2025/10/28
REPOSITORIES: GEO
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Project description:RNA-sequencing of SVF-derived preadipocytes and adipocytes from inguinal white adipose tissue of male mice treated with vehicle, CGRPa, NPY, NE, or SP
| PRJNA1245297 | ENA
Project description:Neuropeptide Y (NPY) is an endogenous modulator of neuronal activity by regulating GABA and glutamate release. Previously, we found that estradiol modulates NPY expression in the hippocampal dentate gyrus. Here we investigated which estrogen receptor type activation is required for the NPY expression. Further, we determined effects of estrogen receptor activation on NPY release. Finally, we determined the contribution of estrogen-mediated remodeling of the GABAergic and glutamatergic network in relation to changes in coupling with NPY in ovariectomized rats. We found that activation of either estrogen receptor type increases NPY expression as well as NPY release in the dentate gyrus. We also found that compared to OVX rats, estrogen replacement increases the likeness of synergistic/antagonistic coupling between the NPY and GABAergic synapse genes while the glutamatergic synapse genes are less likely coupled with NPY. The data together suggest that estrogen plays a critical role in regulation of activity of the NPY system and its coupling to GABAergic and glutamatergic synapses in female rat dentate gyrus. Two-conditions (E = beta-estradiol replacement vs O = oil) experiment. Biological replicates: 4E, 4O.
2014-08-02 | E-GEOD-60013 | biostudies-arrayexpress
Project description:Neuropeptide Y (NPY) is an endogenous modulator of neuronal activity by regulating GABA and glutamate release. Previously, we found that estradiol modulates NPY expression in the hippocampal dentate gyrus. Here we investigated which estrogen receptor type activation is required for the NPY expression. Further, we determined effects of estrogen receptor activation on NPY release. Finally, we determined the contribution of estrogen-mediated remodeling of the GABAergic and glutamatergic network in relation to changes in coupling with NPY in ovariectomized rats. We found that activation of either estrogen receptor type increases NPY expression as well as NPY release in the dentate gyrus. We also found that compared to OVX rats, estrogen replacement increases the likeness of synergistic/antagonistic coupling between the NPY and GABAergic synapse genes while the glutamatergic synapse genes are less likely coupled with NPY. The data together suggest that estrogen plays a critical role in regulation of activity of the NPY system and its coupling to GABAergic and glutamatergic synapses in female rat dentate gyrus.
2014-08-02 | GSE60013 | GEO
Project description:In paravertebral sympathetic ganglia, 50 to 70% of the neurons selectively express neuropeptide Y (NPY). We sought to identify other genes that are differentially expressed by NPY-positive and NPY-negative neurons. This study used NPY reporter mice (B6.FVB-Tg(Npy-hrGFP)1Lowl/J) (Jackson Laboratory #006417) that were bred as hemizygotes with C57BL/6 mice.
2016-05-04 | GSE81075 | GEO
Project description:Neuropeptide Y (NPY) exerts powerful feeding related functions in the hypothalamus. However, NPY is also present in extra-hypothalamic nuclei, however their influence on energy homeostasis is unclear. Here we uncover a previously unknown feeding stimulatory pathway that is activated under conditions of stress in combination with calorie dense food with NPY neurons in the central amygdala (CeA) being responsible for an exacerbated response to a combined stress and high fat diet intervention. CeA NPY neuron specific Npy overexpression mimics the obese phenotype seen in a stress/HFD model, which is prevented by the selective ablation of Npy. Using food intake and energy expenditure (EE) as readout we demonstrate that selective activation of CeA NPY neurons results in increased food intake and a decrease in EE, which requires the presence of NPY. Mechanistically it is the diminished insulin signalling capacity on CeA NPY neurons under stress combined with HFD conditions that leads to the exaggerated development of obesity.
2019-03-31 | GSE128413 | GEO
Project description:BackgroundThe cyclic adenosine-monophosphate (cAMP) pathway is generally recognized as one of the essential pathways for the adipose conversion of rodent preadipocytes in vitro. However, divergent effects of cAMP on adipocyte differentiation have also been reported. Since there is very little data on non-rodent preadipose cells, the aim of the present work was to analyze the effects of one classic activator (dbcAMP) of the cAMP pathway on the proliferation and differentiation of sheep preadipocytes grown.MethodWe retrospectively analyzed the regulation of dbcAMP on the proliferation and differentiation of sheep preadipocytes through observation on cell dynamic morphology, drawing on the growth curve, Oil Red O staining and induction of cell differentiation.Results1) During first 5 days of treatment, at lower levels of dbcAMP (1 nmol/L to 1 × 104 nmol/L), sheep cells were not increased, but at higher levels (1 × 105 nmol/l to 1 × 106 nmol/l), they were significantly increased (P < 0.05); 2) dbcAMP had the trendency to promote cell differentition, but it was not significant (P > 0.05); 3) treated for 4 days, dbcAMP at the levels of 1 nmol/L, 1 × 104 nmol/L and 1 × 106 nmol/L increased C20:0 abundance (P < 0.05), but other fatty acids had no significant changes; 4) treated for 4 days, expression of SCD mRNA had no significant change (P > 0.05), but expression of HSL mRNA increased at the level of 1 × 106 nmol/L dbcAMP (P < 0.05).ConclusionThis study demonstrated that the mechanisms by which of the cAMP pathway affects on preadipocytes between sheep and rodent animals was different.
| S-EPMC5437410 | biostudies-literature
Project description:We used ChIP-seq to identify possible EGR1 (Early growth response 1) binding sites in Npy, Npy1/2/5/r in the dorso-lateral striatum in C57BL/6J mice.
2017-03-30 | E-MTAB-5503 | biostudies-arrayexpress
Project description:Cortical GABAergic interneurons have been shown to fulfil important roles by inhibiting excitatory principal neurons. Recent transcriptomic studies have confirmed seminal discoveries that used anatomical and electrophysiological methods highlighting the existence of multiple different classes of GABAergic interneurons. However, individual studies have rarely addressed regional specific differences in gene expression in a given subclass of neuron. Using single-cell Patch-RNAseq, we characterised neuropeptide Y (NPY)-positive GABAergic interneurons in superficial layers of the primary auditory cortex and in distal layers of area CA3. We found that more than 300 genes are differentially expressed in NPY-positive neurons between these two brain regions. For example, the AMPA receptor auxiliary subunit Shisa9/CKAMP44 and the 5-HT2a receptor are significantly higher expressed in auditory NPY-positive neurons. These findings guided us to perform pharmacological experiments that revealed a role for 5-HT2a receptors in auditory NPY-positive neurons. Specifically, although the application of 5-HT led to a depolarisation of both auditory and CA3 NPY-positive neurons, the 5-HT2a receptor antagonist ketanserin only reversed membrane potential changes in auditory NPY-positive neurons. Our study demonstrates the potential of single-cell transcriptomic studies in guiding directed pharmacological experiments.
2022-04-20 | GSE193293 | GEO
Project description:Gene expression profiles of chicken preadipocytes were constructed using Chicken Genome Arrays to determine the gene expression patterns of preadipocytes derived from two chicken lines divergently selected for abdominal fat content. Oleate was used as an inducer of preadipocyte differentiation, and the different expressed genes between the normal and oleate treated preadipocyte were analyzed.
2016-09-24 | GSE51330 | GEO
Project description:We show that leptin regulates appetite and body weight via PNOC neurons, and that loss of leptin receptor expression in PNOC-expressing neurons in the arcuate nucleus of the hypothalamus (ARC) causes hyperphagia and obesity. Lepr inactivation in PNOC neurons increases Npy expression in a subset of hypothalamic PNOC neurons that do not express Agrp and selective chemogenetic activation of PNOC/NPY neurons promotes feeding to the same extent as activating all PNOCARC neurons and overexpression of Npy in PNOCARC neurons promotes hyperphagia and obesity. Thus, we introduce PNOC/NPYARC neurons as an additional critical mediator of leptin action and a promising target for obesity therapeutics.
2025-04-23 | GSE292416 | GEO