Project description:ACTH is known to be secreted from pituitary cortictropes after CRH and Il-6 stimulation. Recenetly it was proven that eNampt also stimulates ACTH secretion from rat pituitary gland. We used microarrays to detail the global programme of gene expression in isolated rat pituitary corticotropes, 24h after administration of eNampt, CRH and Il-6.
Project description:Primary trophoblast cells were treated with corticotropin releasing hormone (CRH) and then subjected to RNA extraction and sequencing.
Project description:We generated a single nuclei RNA-seq (snRNA-seq) dataset derived from the postnatal hypothalamus of CRH-IRESCre (CRH-Cre) mice using a retrograde Connect-seq approach.
Project description:Rationale: A previous transcriptome meta-analysis revealed significantly lower levels of corticotropin-releasing hormone (CRH) mRNA in corticolimbic brain regions in major depressive disorder (MDD) subjects. Rodent studies show that cortical CRH is mostly expressed in GABAergic neurons; however, the characteristic features of CRH+ cells in human brain cortex and their association with MDD are largely unknown. Methods: Subgenual anterior cingulate cortex (sgACC) of human subjects without brain disorders were labeled using fluorescent in situ hybridization (FISH) for CRH and markers of excitatory (SLC17A7), inhibitory (GAD1) neurons, as well as markers of other interneuron subpopulations (PVALB, SST, VIP). MDD-associated changes in CRH+ cell density and cellular CRH expression (n=6/group) were analyzed. RNA-sequencing was performed on sgACC CRH+ neurons from comparison and MDD subjects (n=6/group), and analyzed for group differences. Results: About 80% of CRH+ cells were GABAergic and 17.5% were glutamatergic. CRH+ GABAergic neurons co-expressed VIP (52%), SST (7%), or PVALB (7%). MDD subjects displayed lower CRH mRNA levels in GABAergic neurons relative to comparison subjects without changes in cell density. CRH+ neurons show transcriptomic profile suggesting lower excitability and less GABA release and reuptake. Further analyses suggested that these molecular changes are not mediated by altered glucocorticoid feedback and potentially occur downstream for a common modulator of neurotrophic function. Summary: CRH+ cells in human sgACC are a heterogeneous population of GABAergic neurons, although largely co-expressing VIP. MDD is associated with reduced markers of inhibitory function of CRH+ neurons.
Project description:Here we translationally profiled the transcriptome of Crh-expressing neurons (Crh neurons) within the CeA following fear conditioning (FC) and fear extinction (EXT) in mice using translating ribosome affinity purification (TRAP) followed by RNA sequencing. A tone alone group (TA) was used as a control group.
Project description:MCF7 cells were stimulated with vehicle or 100nM corticotropin releasing hormone (CRH) for 24h. The effect of CRH on the expression of genes relevant to estrogen signalling was investigated by using the Human Estrogen Receptor Signaling RT² Profiler™ PCR Array (SABioscience Corp).
Project description:The development of atherosclerotic plaque in the arterial intima can cause cardiovascular and cerebrovascular diseases worldwide. Our previous study reported that widespread neuroimmune cardiovascular interfaces appeared in the adventitia of atherosclerotic plaque, establishing a structural artery-brain circuit. Hypothalamic corticotropin-releasing hormone (CRH) neurons play a pivotal role in regulating the stress response and peripheral neuro-immune response. However, it remains unclear whether hypothalamic CRH neurons can regulate atherosclerosis. Elevated levels of sympathetic neurotransmitters and immune cells in the blood of patients with myocardial infarction suggested a role for sympathetic nervous activation in validating and promoting immune cell proliferation. Activation of hypothalamic CRH neurons in ApoE knockout mice promoted atherosclerosis and adventitial inflammation. Single-cell immune repertoire sequencing analysis demonstrated that hypothalamic CRH neurons drove splenic Treg/Teff imbalance via the ADRβ2-MAPK axis and reshaped immune interaction networks to promote early atherosclerotic inflammation. Cell proliferation labeling experiments proved that hypothalamic CRH neurons promoted splenic immune cell proliferation in the early stage of atherosclerosis. Stereotaxic injection of apoptotic viruses to eliminate hypothalamic CRH neurons and surgical ablation of splenic sympathetic signals reduced splenic immune cell proliferation and inflammatory responses, which contributing to the alleviation of atherosclerosis. In summary, our study demonstrates that hypothalamic CRH neurons triggered splenic cell proliferation and promoted atherosclerosis.
Project description:MCF7 cells were stimulated with vehicle or 100nM corticotropin releasing hormone (CRH) for 24h. The effect of CRH on the expression of genes relevant to estrogen signalling was investigated by using the Human Estrogen Receptor Signaling RTM-BM-2 ProfilerM-bM-^DM-" PCR Array (SABioscience Corp). qPCR gene expression profiling. MCF7 cells were treated separately in triplicate. Equal amount total RNA was processed further for gene expression analysis.