Sex and estrogen affect the distribution of urocortin-1 immunoreactivity in brainstem autonomic nuclei of the rat

Ciriello, John

doi:10.1016/j.brainresbull.2015.06.007

Cited by 4 publications

(4 citation statements)

References 86 publications

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“…Another possibility is that parasympathetic preganglionic neurons release Ucn1 (Figure 7B). Ucn1 has been shown to be present in the dorsal motor nucleus of the vagus (DMV) 42 . However, there is little information about Ucn1 in the parasympathetic nerves, and further investigations are therefore necessary.…”

Section: Discussionmentioning

confidence: 99%

Urocortin 1: A putative excitatory neurotransmitter in the enteric nervous system

Yamato

Kurematsu

Amano

et al. 2020

Neurogastroenterology Motil

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Background Urocortin 1 (Ucn1), a stress‐related peptide, is a member of the corticotropin‐releasing factor (CRF) family and acts as a CRF1 receptor agonist. Ucn1 and CRF1 receptor immunoreactivity are present in the enteric nervous system (ENS), and Ucn1 elicits contraction of colonic muscle strips. Considering these findings, we have hypothesized that Ucn1 acts as an excitatory neurotransmitter in the ENS. The present study was conducted to determine whether exogenously applied Ucn1 causes contractions, whether it participates in neurally mediated contraction, and whether it is released from the ENS of the rat colon. Methods Isometric tension of the rat colonic muscle strips (middle to distal colon) in a longitudinal direction was measured. The effects of Ucn1 on phasic contractions were examined in the absence and presence of antalarmin (CRF1 receptor antagonist), tetrodotoxin (TTX), and atropine. The effects of antalarmin on electrical field stimulation (EFS)‐induced contractions were examined in the absence and presence of atropine. Ucn1 peptide in the bath solution was measured after EFS using an EIA kit. Key Results Ucn1 caused a significant and dose‐dependent increase in phasic contractions. These effects were completely inhibited by antalarmin, TTX, and atropine. EFS‐induced contractions were inhibited by antalarmin. Atropine markedly reduced EFS‐induced contractions, and antalarmin did not decrease these contractions further. EFS elicited a significant increase in the concentration of Ucn1 in the bath solution, and this increase was completely inhibited by TTX. Conclusions and Inferences These results suggest that Ucn1 acts as an excitatory neurotransmitter in the ENS enhancing the cholinergic neurotransmission.

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Section: Discussionmentioning

confidence: 99%

Urocortin 1: A putative excitatory neurotransmitter in the enteric nervous system

Yamato

Kurematsu

Amano

et al. 2020

Neurogastroenterology Motil

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“…One possible explanation for this phenomenon is that UCN-1 and sex hormones may be regulated with each other. The sex and estrogen decreased the distribution of UCN-1 in the nucleus of the solitary tract (Ciriello 2015). Deletion of CRHR1, the UCN-1 receptors, selectively impairs maternal, but not intermale aggression (Gammie, Seasholtz, and Stevenson 2008).…”

Section: Discussionmentioning

confidence: 98%

Urocortin-1 Promotes Colorectal Cancer Cells Migration, Proliferation and Inhibits Apoptosis via Inhibition of p53 Signaling Pathway

Guo,

Li,

Chen

et al. 2023

Preprint

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Purpose To investigate the effect of urocortin-1 (UCN-1) on the growth, migration and apoptosis of colorectal cancer (CRC) in vivo and vitro and mechanism of UCN-1 modulating CRC cells in vitro. Methods The correlation between UCN-1 and CRC was evaluated by Cancer Genome Atlas (TCGA) database and the tissues microarray. The expression of UCN-1 in CRC cells was explored by quantitative real-time polymerase chain reaction (RT-qPCR) or western blot. In vitro, the influence of UCN-1 on proliferation, apoptosis and migration HCT-116 and RKO cells were explored by celigo cell counting assay, flow cytometry and wound healing assay or transwell, respectively. In vivo the effect of UCN-1 on CRC tumor growth and progression was evaluated in the nude mice. The downstream pathway behind UCN-1 regulating CRC was found by phospho-kinase profiler array in RKO cells. Expression of UCN-1 in cells was knocked down or upregulated using lentivirus. Results Both of the results of TCGA database and the tissues microarray shown that UCN-1 strongly expressed in tissues of CRC patients. Furthermore, the tissues microarray results showed that expression of UCN-1 was higher in male CRC patients than that in female patients, and high expression of UCN-1 was associated with higher risk of lymphatic metastasis and later pathological stage. Additionally, knockdown of UCN-1 in CRC cells caused a reduction in cell proliferation, migration, and colony formation as well as an increase in apoptosis. In xenograft experiments, tumors generated from RKO cells with UCN-1 knockdown exhibited declined tumor volume and weight. Reduction of the expression of Ki67 in xenograft tumors reflected that knockdown of UCN-1 curbed the growth of CRC tumors. Furthermore, the human phospho-kinase array showed that p53 signal pathway participated in UCN-1-mediated CRC development. The suppression in migration and proliferation caused by UCN-1 knockdown was reversed by inhibitors of p53 signal pathway, while the increase of cell apoptosis was withdrawn. On the other hand, overexpression of UCN-1 promoted the proliferation and migration and inhibited apoptosis of CRC cells. Overexpression of p53 reversed the effect of UCN-1 overexpression on CRC development. Conclusion UCN-1 promotes the migration, proliferation and inhibits apoptosis via inhibition of p53 signaling pathways.

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“…Under normal physiological conditions, female mice have lower plasma VTN levels than males, which would be consistent with the findings that the vagus nerve normally has a higher tone in women (Abhishekh et al, 2013 ) and female rats (Du et al, 1994 ). The vagal brainstem nuclei have sexual dimorphisms (Akmayev et al, 1994 ; Ciriello, 2015 ; Dergacheva, 2015 ), including different urocortin‐1 positive innervation patterns (Ciriello, 2015 ). Urocortin‐1 injection can activate the vagus nerve (Chitravanshi et al, 2013 ) but it is unclear how this would be involved in regulating different baseline liver VTN expression levels in females and males.…”

Section: Discussionmentioning

confidence: 99%

“…Hepatocytes have muscarinic cholinergic receptors (Li et al, 2009 ; Vatamaniuk et al, 2003 ). The female human (Abhishekh et al, 2013 ) and rat (Du et al, 1994 ) vagus nerve normally have a higher tone relative to males, and vagal brainstem nuclei have sexual dimorphisms (Akmayev et al, 1994 ; Ciriello, 2015 ; Dergacheva, 2015 ). Whether and how vagal tone may affect the expression of liver vitronectin has not been studied.…”

Section: Introductionmentioning

confidence: 99%

Liver vitronectin release into the bloodstream increases due to reduced vagal muscarinic signaling after cerebral stroke in female mice

Keasey

Lovins

Jia

et al. 2022

Physiological Reports

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Vitronectin (VTN) is a glycoprotein enriched in the blood and activates integrin receptors. VTN blood levels increase only in female mice 24 h after an ischemic stroke and exacerbate brain injury through IL‐6‐driven inflammation, but the VTN induction mechanism is unknown. Here, a 30 min middle cerebral artery occlusion (MCAO) in female mice induced VTN protein in the liver (normally the main source) in concert with plasma VTN. Male mice were excluded as VTN is not induced after stroke. MCAO also increased plasma VTN levels after de novo expression of VTN in the liver of VTN−/− female mice, using a hepatocyte‐specific (SERPINA1) promoter. MCAO did not affect SERPINA1 or VTN mRNA in the liver, brain, or several peripheral organs, or platelet VTN, compared to sham mice. Thus, hepatocytes are the source of stroke‐induced increases in plasma VTN, which is independent of transcription. The cholinergic innervation by the parasympathetic vagus nerve is a potential source of brain‐liver signaling after stroke. Right‐sided vagotomy at the cervical level led to increased plasma VTN levels, suggesting that VTN release is inhibited by vagal tone. Co‐culture of hepatocytes with cholinergic neurons or treatment with acetylcholine, but not noradrenaline (sympathetic transmitter), suppressed VTN expression. Hepatocytes have muscarinic receptors and the M1/M3 agonist bethanechol decreased VTN mRNA and protein release in vitro via M1 receptors. Finally, systemic bethanechol treatment blocked stroke‐induced plasma VTN. Thus, VTN translation and release are inhibited by muscarinic signaling from the vagus nerve and presents a novel target for lessening detrimental VTN expression.

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Sex and estrogen affect the distribution of urocortin-1 immunoreactivity in brainstem autonomic nuclei of the rat

Cited by 4 publications

References 86 publications

Urocortin 1: A putative excitatory neurotransmitter in the enteric nervous system

Urocortin 1: A putative excitatory neurotransmitter in the enteric nervous system

Urocortin-1 Promotes Colorectal Cancer Cells Migration, Proliferation and Inhibits Apoptosis via Inhibition of p53 Signaling Pathway

Liver vitronectin release into the bloodstream increases due to reduced vagal muscarinic signaling after cerebral stroke in female mice

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