Relevant bibliographies by topics / Urotensin II

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Academic literature on the topic 'Urotensin II'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Urotensin II"

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Giuliani, Luisa, Livia Lenzini, Michele Antonello, Enrico Aldighieri, Anna S. Belloni, Ambrogio Fassina, Celso Gomez-Sanchez, and Gian Paolo Rossi. "Expression and Functional Role of Urotensin-II and Its Receptor in the Adrenal Cortex and Medulla: Novel Insights for the Pathophysiology of Primary Aldosteronism." Journal of Clinical Endocrinology & Metabolism 94, no. 2 (February 1, 2009): 684–90. http://dx.doi.org/10.1210/jc.2008-1131.

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Abstract Context: The involvement of urotensin II, a vasoactive peptide acting via the G protein-coupled urotensin II receptor, in arterial hypertension remains contentious. Objective: We investigated the expression of urotensin II and urotensin II receptor in adrenocortical and adrenomedullary tumors and the functional effects of urotensin II receptor activation. Design: The expression of urotensin II and urotensin II receptor was measured by real time RT-PCR in aldosterone-producing adenoma (n = 22) and pheochromocytoma (n = 10), using histologically normal adrenocortical (n = 6) and normal adrenomedullary (n = 5) tissue as control. Urotensin II peptide and urotensin II receptor protein were investigated with immunohistochemistry and immunoblotting. To identify urotensin II-related and urotensin II receptor-related pathways, a whole transcriptome analysis was used. The adrenocortical effects of urotensin II receptor activation were also assessed by urotensin II infusion with/without the urotensin II receptor antagonist palosuran in rats. Results: Urotensin II was more expressed in pheochromocytoma than in aldosterone-producing adenoma tissue; the opposite was seen for the urotensin II receptor expression. Urotensin II receptor activation in vivo in rats enhanced (by 182 ± 9%; P < 0.007) the adrenocortical expression of immunoreactive aldosterone synthase. Conclusions: Urotensin II is a putative mediator of the effects of the adrenal medulla and pheochromocytoma on the adrenocortical zona glomerulosa. This pathophysiological link might account for the reported causal relationship between pheochromocytoma and primary aldosteronism.
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Desai, Nirav, Jameel Sajjad, and William H. Frishman. "Urotensin II." Cardiology in Review 16, no. 3 (May 2008): 142–53. http://dx.doi.org/10.1097/crd.0b013e31815c8048.

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Giebing, G., M. Tölle, S. Schmidt, A. Oksche, W. Zidek, and M. Van Der Giet. "UROTENSIN II-RECEPTORS SHOW RAPID DESENSITIZATION AFTER STIMULATION WITH UROTENSIN II." Journal of Hypertension 22, Suppl. 2 (June 2004): S48. http://dx.doi.org/10.1097/00004872-200406002-00161.

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Dubessy, Christophe, Dorthe Cartier, Benoît Lectez, Christine Bucharles, Nicolas Chartrel, Maïté Montero-Hadjadje, Patrice Bizet, et al. "Characterization of urotensin II, distribution of urotensin II, urotensin II-related peptide and UT receptor mRNAs in mouse: evidence of urotensin II at the neuromuscular junction." Journal of Neurochemistry 107, no. 2 (August 14, 2008): 361–74. http://dx.doi.org/10.1111/j.1471-4159.2008.05624.x.

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Lafta, Israa A., Nahla A. AL-Bakri, and Wasan A. Abdulhameed. "Expression of Urotensin II of Human Placental Tissues and in Serum in Gestational Diabetic Mellitus in Iraqi Woman." INTERNATIONAL JOURNAL OF DRUG DELIVERY TECHNOLOGY 12, no. 01 (June 25, 2022): 70–73. http://dx.doi.org/10.25258/ijddt.12.1.13.

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The placenta is an organ between the mother and fetus necessary for fetal growth and development. Gestational diabetes mellitus (DM) is the most frequent metabolic condition detected during pregnancy. It is characterized as hyperglycemia of various severity with onset or first detection during pregnancy that does not clearly describe any form of preexisting diabetes. Urotensin II (UII), a pluripotent vasoactive peptide, is important in developing insulin resistance. This study aimed to determine the level of Urotensin II(UII) in placenta and in the serum of diabetic and nondiabetic women. Methods The blood and placenta tissue collected from 50 ladies had been enrolled in this research ( 25 females with uncomplicated), (25 women with gestational diabetes). Immunohistochemistry (IHC) was used to look at the expression of the Urotensin II (UII) marker in placenta specimens. The IHC analysis revealed that Urotensin II expression was primarily found in placental cytotrophoblast and the syncytiotrophoblast. Results of an immunohistochemistry investigation using the Urotensin II (UII) marker revealed a significant increase (p ≤ 0.001) in diabetic women’s placentas and serum than control groups. Conclusion, the Urotensin II is mainly located in the cytotrophoblast and syncytiotrophoblast. That was significantly higher in the gestational DM group.
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Itoh, H., and K. Lederis. "Relationship of urotensin I induced vasodilatory action in rat thoracic aorta to Ca2+ regulation." Canadian Journal of Physiology and Pharmacology 65, no. 3 (March 1, 1987): 298–302. http://dx.doi.org/10.1139/y87-052.

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The relaxant effects of the synthetic fish neuropeptide urotensin I were examined in helical strips of rat aorta. In K+-depolarized aorta strips, urotensin I and verapamil competitively inhibited Ca2+-induced contractions. Urotensin I relaxed, in a concentration-dependent manner, the contraction produced by the Ca2+ ionophore A23187, whereas verapamil had no effect on this contraction, even at a concentration of 10−5 M. In the absence and presence of extracellular Ca2+, urotensin I inhibited both components of the contractions elicited by norepinephrine or urotensin II, another fish neuropeptide. Verapamil reduced only the norepinephrine or urotensin II induced contraction in the presence of extracellular Ca2+, with little or no change in the contraction in Ca2+-free buffer. The urotensin I induced relaxation response in aortic strips contracted by 40 mM KCl was enhanced by pretreatment with papaverine or forskolin. Pretreatment with dibutyryl cAMP did not significantly alter the action of urotensin I. The presence or absence of endothelial cells did not change the response to urotensin I. These results suggest that urotensin I antagonizes the action and (or) mobilization of extracellular and intracellular Ca2+.
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Strack, Martin, Étienne Billard, David Chatenet, and William D. Lubell. "Urotensin core mimics that modulate the biological activity of urotensin-II related peptide but not urotensin-II." Bioorganic & Medicinal Chemistry Letters 27, no. 15 (August 2017): 3412–16. http://dx.doi.org/10.1016/j.bmcl.2017.05.088.

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Carotenuto, A., P. Grieco, P. Rovero, and E. Novellino. "Urotensin-II Receptor Antagonists." Current Medicinal Chemistry 13, no. 3 (February 1, 2006): 267–75. http://dx.doi.org/10.2174/092986706775476061.

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Loirand, Gervaise, Malvyne Rolli-Derkinderen, and Pierre Pacaud. "Urotensin II and atherosclerosis." Peptides 29, no. 5 (May 2008): 778–82. http://dx.doi.org/10.1016/j.peptides.2007.08.024.

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Hazon, N., C. Bjenning, and J. M. Conlon. "Cardiovascular actions of dogfish urotensin II in the dogfish Scyliorhinus canicula." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 3 (September 1, 1993): R573—R576. http://dx.doi.org/10.1152/ajpregu.1993.265.3.r573.

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Bolus injections of synthetic dogfish urotensin II (0.1-1.0 nmol) into the celiac artery of the conscious dogfish Scyliorhinus canicula (n = 8) resulted in sustained and dose-dependent increases in arterial blood pressure and pulse pressure. A maximum rise in mean arterial pressure of 10.5 +/- 1.2 mmHg (equivalent to 38.6 +/- 4.2% over mean basal values) and a maximum increase in pulse pressure of 3.9 +/- 0.8 mmHg was elicited by injection of 0.5 nmol of peptide. In comparison, a bolus injection of epinephrine (5 nmol) elicited a rise of 24.8 +/- 3.3% in mean arterial pressure. Bolus injection of 0.5 nmol synthetic goby (Gillichthys mirabilis) urotensin II under the same conditions did not elicit a significant hypertensive response. When dogfish urotensin II (0.5 nmol) was administered 3 min after an intra-arterial injection of phentolamine, the rise in arterial blood pressure was completely abolished. Dogfish urotensin II produced a dose-dependent contraction (pD2 = 6.58 +/- 0.07; n = 8) of isolated rings of vascular muscle prepared from the first afferent branchial artery of the dogfish. A maximum contractile force of 1.3 mN was produced by 10(-5) M peptide. The urotensin II-induced contraction of the vascular rings was unaffected by pretreatment with tetrodotoxin (1 microM) or indomethacin (14 microM). It is concluded that urotensin II has potent hypertensive activity in the dogfish that is mediated, at least in part, through release of catecholamines, but the sustained nature of the pressor response suggests that the peptide may have a direct action on the heart.
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Dissertations / Theses on the topic "Urotensin II"

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Batuwangala, Madura Suharshana. "Human urotensin-II receptor desensitisation." Thesis, University of Leicester, 2009. http://hdl.handle.net/2381/7846.

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Human Urotensin-II (U-II) is a cyclic undecapeptide that binds to the U-II receptor UT. The desensitisation mechanisms of the UT receptor (G_{q/11} coupled GPCR) are not well defined and hampered by (1) lack of native (in-vitro) models; (2) paucity of ligands, especially non-peptides and (3) irreversible binding of U-II. There are some limited studies using rat aorta, where a U-II induced primary contractile response was reduced upon a secondary re-challenge after 5-hours. Studies were undertaken to characterise cell lines expressing native (SJCRH30) and recombinant human hUT (HEK293 and CHO) for their suitability in binding and functional assays (PI and Ca^2+). SAR studies were carried out to characterise novel analogues modified at Tyr^9 of the U-II(4-11) template. This led to the identification of [3,5-diiodoTyr^9]U-II(4-11) a partial agonist in aorta and Ca^2+ assays at rat UT. Full agonism was demonstrated at hUT in PI and Ca^2+ assays. Efforts were made to delineate functional and genomic desensitisation of hUT. There was no functional desensitisation in SJCRH30. In HEK293hUT functional heterologous desensitisation of hUT was observed, this was not so in CHOhUT; instead P_2YR was functionally attenuated. In SJCRH30 6-hr U-II treatments led to UT mRNA reduction. Genomic desensitisation was also studied in Peripheral blood mononuclear cells (PBMCs). U-II treatments alone did not affect UT mRNA. Lipolysaccharide treatment of PBMCs led to UT mRNA upregulation which was desensitised with U-II treatments. In recombinant systems UT mRNA was upregulated at 6-hr U-II treatments. In conclusion modification of the U-II(4-11) template at Tyr^9 is useful for reducing efficacy. There is a difference in desensitisation profiles of native and recombinant hUT, where native receptors are not prone to functional desensitisation while receptor mRNA is reduced. In recombinant systems, hUT undergoes desensitisation (HEK293hUT only) while receptor mRNA is increased in both systems.
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Ong, Kwok-leung. "Metabolic syndrome its prevalence and association with urotensin II /." Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B3723058X.

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Ong, Kwok-leung, and 王國良. "Metabolic syndrome: its prevalence and association with urotensin II." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B3723058X.

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Eyre, Heather. "Urotensin II in the development of experimental chronic kidney disease." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/urotensin-ii-in-the-development-of-experimental-chronic-kidney-disease(e12bed8b-1bef-4bd1-9b19-5546ce7e1af9).html.

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Urotensin II (UII) is a potent peptide hormone with a complex species and vessel-dependent vascular profile. UII and the homologous UII-related peptide (URP) bind to the g-protein coupled urotensin II receptor (UT) with high affinity. The peptide ligands and receptor have been detected in numerous human and rat tissues including heart, brain and kidney. The kidney is a major source of UII, which appears to act as both an endocrine and paracrine mediator of renal function. UII has been shown to influence renal blood flow, glomerular filtration rate and sodium handling in the renal tubules. More speculative actions of UII as a pro-fibrotic mediator include the activation of fibroblasts and promotion of collagen synthesis. Abnormally elevated UII, URP and UT expression has been highlighted in a number of cardio-renal disease states; particularly end stage renal disease, diabetes and diabetic nephropathy (DN). This work aims to investigate the role of the UII system in the development and progression of CKD using an experimental model of CKD in rodents. The first aim of the current work involved establishing the surgical 5/6th subtotal nephrectomy (SNx) model of chronic kidney disease (CKD) in the laboratory and forming a profile of UII expression in late stage experimental CKD to complement UII clinical data which are exclusively from patients in the later stages of disease. UII/URP and UT were substantially over-expressed in the kidneys of SNx rats in late stage CKD. This novel insight complements the clinical profile of CKD/DN where over expression of the UII system is routinely reported. In a second study the 5/6th SNx rat model was used to explore the effects of chronic UT receptor antagonism on the progression of CKD. Although there were no discernible differences in kidney mass or histological profile between the treatment groups at the end of the study, there was a small delay in the development of albuminuria and in the onset of systolic blood pressure elevation in the UT antagonist treated cohort. The study did not produce clear-cut evidence defining the potential therapeutic value of UT-antagonism in the treatment of CKD. Despite this the results are encouraging and suggest that the role of UT-inhibition in CKD is worth considering further.
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Affolter, Jonathan Theodore. "Vasoactive hormone studies in man using urotensin II and vasopressin." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/28010.

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Using the established method of bilateral venous occlusion plethysmography to measure forearm blood flow, combined with intra-arterial infusion of drugs into the brachial artery, we sought to determine the effects of urotensin II on human forearm blood flow. Other methods such as the Aellig venous displacement technique, to assess venous tone, and pulse wave analysis, to quantify arterial stiffness were also used during local and systemic urotensin II intravenous infusions respectively. Doppler flowmetry was used to assess skin microcirculation combined with intra-dermal peptide injection respectively. Doppler flowmetry was used to assess skin microcirculation combined with intra-dermal peptide injection; we assessed skin blood flow in response to vasopressin alone and in combination with a novel selective VI antagonist. Venous occlusion plethysmography was again used to determine forearm blood flow responses to vasopressin alone and in combination with V1 and V2 antagonists. During intra-arterial infusion of urotensin II we did not observe any significant changes in forearm blood flow, even in the presence of endothelial inhibitors such as aspirin and a ‘nitric oxide clamp’ nor was change observed in venous tone. Moreover, no alteration in systemic haemodynamics or arterial stiffness was seen during systemic intravenous infusion. We observed a significant fall in skin blood flow with intra-dermal injection of vasopressin, however, the V1 receptor antagonist did not alter skin vasoconstriction. Intra-arterial infusion of vasopressin caused a reproducible biphasic change in forearm blood flow, low doses causing vasoconstriction and high doses, nitric oxide mediated vasodilatation. Vasodilatation was subject to tachyphylaxis during prolonged infusion of high dose vasopressin. Neither intra-arterial V1 or V2 antagonist, when co-infused with vasopressin, altered this biphasic vasoconstriction and vasodilatation.
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Bousette, Nicolas. "The role of urotensin-II in atherosclerosis and ischemic cardiomyopathy /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111848.

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Atherosclerosis, a vascular disease which may lead to coronary artery occlusion and consequent myocardial infarction is primarily caused by dyslipidemia. Ischemic cardiomyopathy due to atherosclerosis is the leading cause of morbidity and mortality in the western world today. Vasoactive factors are increasingly being recognized not only as contributors to atherosclerotic plaque formation, but also to cardiac function and remodeling following ischemic cardiac injury. Urotensin II (UII) is one such vasoactive factor. UII possesses a wide range of cardiovascular effects, from contraction of the rat aorta to complete cardiovascular collapse in cynomolgus monkeys. UII binds a seven transmembrane spanning G-protein coupled receptor termed UT. Expression of UII is significantly elevated in the hearts of patients with congestive heart failure (CHF). Recent reports have also shown increased plasma levels of the peptide in patients with CHF, and these levels correlated with the severity of the disease. This project was designed to investigate the role of UII and UT in both atherosclerosis and CHF. To this end, UII expression was evaluated both in a model of CHF in the rat, and in human atherosclerosis of the carotid arteries and aortae. Furthermore, the pathophysiological role of urotensin-I1 in CHF was investigated, with the use of a selective UII antagonist, SB-611812. Finally, genetically modified mice deficient in either ApoE, UT, or both genes, were evaluated to study the role of UII/UT signaling in a model of atherosclerosis. We found that UII and its receptor, UT, were both significantly elevated in a model of CHF induced by coronary artery ligation. UII antagonism significantly attenuated mortality, cardiac dysfunction, and hypertrophy. This was associated with a significant decrease in cardiac fibrosis. We next went on to demonstrate that UII and UT were significantly elevated in human atherosclerotic carotid arteries and aortae. Finally, we demonstrated that deletion of the UT gene in mice deficient for ApoE exacerbates atherosclerosis of the aorta. Furthermore, this was associated with significantly increased hyperlipidemia and organ hypertrophy as well as significantly reduced body mass, liver mass, and hepatic steatosis.
In conclusion we were the first to demonstrate a pathophysiological role for UII in cardiovascular diseases which may lead to a breakthrough in the management of CHF and may also give more insight into the pathogenesis of atherosclerosis.
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Ahmed, Shenge [Verfasser]. "Suche, Reinigung und Identifizierung eines Urotensin II metabolisierenden Enzyms / Shenge Ahmed." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2010. http://d-nb.info/1024335186/34.

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menegolo, mirko. "Human primary aldosteronism: from clinical observations to in-vivo and ex-vivo studies on the pressor effects of Urotensin II." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3426182.

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In a patient affected by primary aldosteronism we have identified the presence of a pheochromocytoma not secreting catecholamines. The analysis of the transcriptome in the pheochromocytoma revealed a high expression of Urotensin II (UII). UII is a somatostatin-like cyclic 11-aminoacid vasoconstrictor peptide, first identified in the teleost fish caudal-neuro-secretory system and then in humans, that has been demonstrated to be a potent vasoactive peptide involved in the physiology and pathophysiology of the cardiovascular system through mechanisms still largely unknown. Its action is now the subject of intensive studies on the effects it produces in different animal models and in different vascular beds. The direct effects on the myocardium such as ventricular hypertrophy, increased extracellular matrix and reduction of myocardial contractility suggest a role of UII in cardiac remodelling after myocardial infarction and heart failure. Even if the effects on cardiovascular system are still controversial UII has attracted considerable scientific interest aimed to investigate on its pathophysiology and on its the mechanism of action. We investigated among the expression of UII and its receptor in human adrenal glands and in different adrenal tumors. The opposite trend of expression of UII receptor obtained between aldosterone-producing adenoma and pheocromocitoma, along with the differences of genes implicated in UII signaling, supported a role of UII in the paracrine interactions between the adrenal medulla and cortex. Being relevant for the regulation of adrenal gland function and for the pathophysiology of pheocromocitoma and aldosterone-producing adenomas, these interactions might provide a mechanistic explanation for the pheocromocitomas that presented clinically as aldosteronism. We tested the “in vivo” effects of UII on blood pressure in rats, showing a delayed transient hypertensive effect that resembles the pressure trend in chronic infusion of aldosterone. Thus further supporting the hypothesis of a close interaction between UII and the renin-angiotensin-aldosterone system or even that UII acts through production of aldosterone as well as assess its hypertensive activity, its effect of cardiac hypertrophy and fibrosis and its role in regulating the growth of adrenocortical cells in rats. Considering that the mechanisms involved in the so called “escape phenomenon” seem responsible of the peculiar blood pressure trend in hyperaldosteronism we tested the blood pressure modifications in chronic infusion of UII counteracting the “escape phenomenon” through unilateral nephrectomy, high salt diet and concomitant infusion of spironolactone. The results obtained were promising: for the first time was shown an in-vivo not transient but continuous hypertensive effect of UII. The evidences obtained in blood pressure modification during chronic infusion of UII combined with the ones regarding UII and development of cortical tumors, has taken a step forward in identifying the mechanism of action of UII supporting the hypothesis of a possible close communication between medulla and adrenal cortex and a possible action of UII mediated by aldosterone. Additional investigations on the transgenic rat overexpressing UII in adrenal medulla will certainly contribute to verify our hypothesis.
In una paziente affetta da iperaldosteronismo primario abbiamo identificato la presenza di un feocromocitoma non secernente catecolamine. L’analisi del transcrittoma nel feocromocitoma ha rivelato un’elevata espressione di Urotensina II (UII). L’UII è un peptide ciclico di 11 aminoacidi, identificato inizialmente nel sistema neurosecretorio dei pesci teleostei e successivamente nell’uomo, che oggi è ritenuto un potentissimo vasocostrittore coinvolto nella fisiologia e nella fisiopatologia del sistema cardiovascolare i cui meccanismi di azione sono tuttora largamente sconosciuti. Molti studi su diversi modelli animali, sia in-vitro che in-vivo, hanno documentato che l’UII può indurre ipertrofia cardiaca, aumento della matrice extracellulare e riduzione della contrattilità miocardica, suggerendo una sua possibile implicazione nel rimodellamento cardiaco post-ischemico o nell’insufficienza cardiaca. Nonostante i suoi effetti sul cuore e sull’omeostasi pressoria siano tuttora controversi si è generato un notevole interesse nell’identificazione del ruolo fisiologico dell’UII e dei suoi meccanismi d’azione. Abbiamo studiato l’espressione dell’UII e del suo recettore nel contesto delle ghiandole surrenaliche e in diversi tumori surrenalici constatando un andamento pressochè opposto circa l’espressione di UII e del suo recettore tra feocromocitoma ed adenoma secernente aldosterone: nel feocromocitoma si è documentato un più alto contenuto di di UII rispetto all’adenoma secernente aldosterone che, viceversa, ha mostrato una maggiore espressione del recettore, suggerendo una down-regulation recettoriale secondaria alla produzione di UII. Queste evidenze suggeriscono un ruolo importante dell’UII nelle interazioni paracrine tra midollare e corticale surrenalica e nella fisiopatologia del pheocromocitoma e dell’adenoma secernente aldosterone, dando peraltro una spiegazione meccanicistica per quei feocromocitomi che si presentano clinicamente con iperaldosteronismo. Abbiamo inoltre testato in vivo l’effetto dell’UII sulla pressione arteriosa mediante la sua infusione cronica nel ratto documentando un andamento pressorio molto simile a quello che si ottiene nell’infusione cronica di aldosterone e caratterizzato da un iniziale effetto ipertensivo seguito da un adattamento pressorio verso i valori di partenza. Questo supporta ulteriormente l’ipotesi di stretta interazione tra UII e sistema renina-angiotensina-aldosterone o addirittura di un’azione dell’UII mediata dalla produzione di aldosterone. A questo proposito, partendo dal presupposto che il peculiare andamento pressorio negli stati di iperaldosteronismo è pesantemente influenzato dagli adattamenti di volume che si verificano grazie al fenomeno renale di “escape” abbiamo voluto verificare se vi fossero cambiamenti significativi nell’andamento pressorio durante l’infusione cronica di UII e la concomitante soppressione del meccanismo di escape. I risultati sono stati sorprendenti visto che per la prima volta si è documentato in vivo un effetto ipertensivo, non solo transitorio ma continuativo, dell’UII. Le evidenze ottenute, sia per quel che riguarda gli effetti dell’UII sulla pressione arteriosa che sullo sviluppo dei tumori surrenalici, sicuramente consentono di fare un passo in avanti circa l’identificazione del meccanismo d’azione a sostegno dell’ipotesi che l’UII possa agire come mediatore tra midollare e corticale surrenalica o mediante la produzione stessa di aldosterone. Gli studi in cui prevediamo di utilizzare ratti transgenici per l’espressione di UII nella midollare surrenalica potranno contribuire a confermare o confutare la nostra ipotesi.
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Egginger, Johann-Günther. "Les urotensines dans le système nerveux central : de l'urotensine-II spinale à un nouveau neuropeptide endocrine, l'URP (urotensin-II-related peptide) : approche cytofonctionnelle chez la souris et le rat." Paris 6, 2006. http://www.theses.fr/2006PA066257.

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En 2003, un peptide apparenté à l’urotensine-II (UII), l’urotensin-II-related peptide (URP), a été isolé à partir d’extraits de cerveau de rat. Dans l’hypothèse de l’existence de marqueurs communs aux motoneurones et aux neurones endocrines, nous avons étudié l’expression centrale des gènes de l’UII et de l’URP chez la souris et le rat. Par une approche cytofonctionnelle, nous avons montré que ces deux peptides ainsi que leurs ARNm sont exprimés au sein de motoneurones appartenant à la moelle épinière et particulièrement au niveau lombo-sacré ; l’URP est aussi localisé dans des fibres de l’éminence médiane et au niveau de l’OVLT, ainsi que dans des corps cellulaires appartenant notamment à l’aire préoptique, co-localisé avec la GnRH ; l’URP a une action sur la sphère uro-génitale. Ces résultats montrent que l’URP est non seulement un marqueur motoneuronal mais aussi un nouveau neuropeptide endocrine co-localisé avec la GnRH, et à fonction sexuelle centrale et périphérique
In 2003, a peptide related to urotensin-II (UII), the urotensin-II-related peptide (URP), was isolated from rat brain extracts. On the assumption of the existence of common markers to the motoneurons and the endocrine neurons, we studied the central expression of the genes of UII and URP in the mouse and the rat. By a cytofunctionnal approach we showed that these peptides and their ARNm are expressed within spinal cord motoneurons and particularly at the lumbo-sacral level; URP is also located in the fibers of the median eminence and of the OVLT area, as well as in cell bodies belonging in particular to the preoptic area, co-localized with GnRH; URP has an action on the urogenital sphere. These results show that URP is not only a motoneuronal marker but also a novel neuroendocrine peptide co-localized with GnRH, with a central and peripheral sexual function
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Sorato, Elisa. "Attività pro-angiogenica di urotensina-II su cellule endoteliali vascolari umane." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3427531.

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Urotensin-II (U-II) is a cyclic peptide, originally isolated from the urophysis of the goby Gillichthys mirabilis. The human form of U-II (hU-II) is a cyclic undecapeptide. Mature hU-II is synthesized from a large precursor molecule, the prepro-U-II, whose mRNA has been found in many tissues. U-II has been identified as the endogenous ligand of a specific high-affinity receptor, recently identified as the orphan receptor GPR14 which has been renamed urotensin receptor (UT). The human UT isoform belongs to the class A superfamily of G-protein-coupled receptors. The principal physiological role of U-II in mammals is in the cardiovascular system, where it exerts a potent systemic vasoconstrictor and hypertensive effect and several lines of evidence suggested that U-II might be involved in the pathophysiology of the cardiovascular system. On endothelial cells (EC) of animal origin U-II has also been shown to exert a clearcut pro-angiogenic effect, but few experimental data are presently available clarifying the effect of U-II in human endothelium. Thus, in the present study in vitro models based on human vascular endothelial cells directly isolated from different normal human vessels, including saphenous vein (HSVEC), jugular vein (HJVEC), umbilical vein (HUVEC) and aorta (HAEC) have been used to characterize different aspects of the pro-angiogenic profile exhibited by U-II. RT-PCR and ICC analyses indicated that UT was expressed by all the human EC considered, while the expression of U-II resulted heterogeneous, in fact the peptide was detectable in HAEC and HUVEC only. When tested in the Matrigel assay all the investigated EC exhibited a strong angiogenic response to the peptide, with the formation of a meshwork of capillary-like structures of increased density and complexity when compared to the unstimulated condition. The effect was comparable to that of FGF-2 and was counteracted by Palosuran, a specific antagonist of UT, indicating that they were triggered by the binding of U-II to its receptor. Interestingly, in EC derived from adult vessels this activity was not associated with a proliferogenic effect. On the contrary, U-II induced a moderate but significant increase of cell proliferation in HUVEC. Experiments performed in the presence of specific inhibitors of various steps of the signaling cascade showed that the U-II induced self organization of the cells in capillary-like structures is PKC dependent and involves the activation of the ERK1/2 transduction pathway. Western blot analyses on the phosphorilated forms of these kinases provided further support to this finding. Interestingly, the pharmacological inhibition of PI3K, hindered the capacity of U-II to induce a pro-angiogenic effect on HUVEC, indicating that the PI3K/Akt pathway is also involved in regulating the process. It has also to be observed that some of the signalling pathways activated as a consequence of the binding of U-II to UT can, in principle, be started in several ways. In fact GPCR can also indirectly activate them by inducing the synthesis and release of growth factors. In this respect, the stimulation of HUVEC with U-II for 24 hours, induced AM, ET-1 and VEGF expression, as mRNA and proteins. All these factors are characterized by well known pro-angiogenic properties. Therefore U-II can also act indirectly by stimulating in HUVEC the expression of other pro-angiogenic factors. Altogether, the results of the present study suggested that U-II, in addition to regulating cardiovascular function, also exerts a direct action on the development and remodelling of the vascular network.
Urotensina-II (U-II) è un peptide ciclico, originariamente isolato dall’urofisi del pesce Gillichthys mirabilis, la cui isoforma umana (hU-II) è costituita di 11 aminoacidi. hU-II matura è sintetizzata da un precursore più grande, la prepro-U-II, il cui mRNA è stato individuato in vari tessuti. U-II è stata identificata quale ligando endogeno di uno specifico recettore ad alta affinità, il recettore orfano GPR14 che è stato successivamente rinominato UT. L’isoforma umana di UT appartiene alla classe A della superfamiglia di recettori accoppiati alle proteine G (GPCR). Il principale ruolo fisiologico di U-II nei mammiferi si esplica a livello del sistema cardiovascolare, dove il peptide esercita un notevole effetto ipertensivo e vasocostrittore e proprio per questo molti dati suggeriscono che U-II possa essere coinvolta nella regolazione del sistema cardiovascolare in condizioni sia fisiologiche che patologiche. In cellule endoteliali (EC) di origine animale sembra esercitare un chiaro effetto pro-angiogenico, ma pochi dati sperimentali sono attualmente disponibili per chiarire le azioni del peptide sull’endotelio vascolare umano. In questo lavoro modelli in vitro basati sull’uso di cellule endoteliali vascolari umane isolate direttamente da vasi diversi, quali vena safena (HSVEC), vena giugulare (HJVEC), vena ombelicale (HUVEC) e aorta (HAEC), sono stai utilizzati per caratterizzare vari aspetti del profilo pro-angiogenico di U-II. Analisi di RT-PCR ed immunocitochimica indicano che UT è espresso da tutte le EC umane considerate, mentre l’espressione di U-II risulta eterogenea, infatti il peptide si ritrova solo nelle HUVEC e nelle HAEC. Sottoposte a coltura su Matrigel, tutte le EC analizzate presentano una forte risposta angiogenica al peptide, con conseguente formazione di una rete di strutture capillaro-simili di maggiore densità e complessità rispetto alla situazione di controllo. L’effetto è comparabile a quello indotto da FGF-2 ed è antagonizzato da Palosuran, antagonista specifico di UT, ad indicare che l’attività del peptide è innescata dal legame con il suo recettore funzionale. E’ stato interessante notare che nelle EC derivate da vasi adulti questa azione non è associata ad un effetto proliferativo. Al contrario, U-II induce un moderato ma significativo aumento della proliferazione cellulare nelle HUVEC. Esperimenti condotti in presenza di specifici inibitori di vari step della cascata di segnalazione intracellulare dimostrano che l’auto-organizzazione in strutture capillaro-simili delle EC indotta da U-II è PKC-dipendente e coinvolge l’attivazione del pathway di trasduzione di ERK1/2. Analisi di western blot sulle forme fosforilate di queste chinasi hanno confermato i dati ottenuti con il Matrigel. Inoltre, l’inibizione farmacologica di PI3K, ostacola la capacità di U-II di indurre un effetto pro-angiogenico nelle HUVEC, indicando che anche il pathway PI3K/Akt potrebbe essere coinvolto nella regolazione del processo. E’ da considerare che alcuni pathway attivati come conseguenza del legame di U-II ad UT, potrebbero essere innescati in diversi modi. Infatti, i GPCR potrebbero anche attivarli indirettamente inducendo la sintesi ed il rilascio di fattori di crescita. A questo proposito, si è messo in evidenza come, dopo 24 ore di stimolazione, U-II induca nelle HUVEC l’espressione di AM, ET-1 e VEGF, tutti fattori con proprietà pro-angiogeniche note. A tempi più lunghi, quindi, U-II potrebbe anche agire indirettamente stimolando nelle HUVEC l’espressione di altri fattori pro-angiogenici. I risultati di questo lavoro suggeriscono quindi che U-II, oltre a regolare la funzionalità cardiovascolare, potrebbe anche esercitare un’azione diretta sullo sviluppo e il rimodellamento vascolare.
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Book chapters on the topic "Urotensin II"

1

Albanese, Isabella, and Adel Schwertani. "Circulating Vasoactive Peptide Urotensin II and Relationships with Cardiovascular Disease." In Biomarkers in Cardiovascular Disease, 153–75. Dordrecht: Springer Netherlands, 2016. http://dx.doi.org/10.1007/978-94-007-7678-4_6.

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Albanese, Isabella, and Adel Schwertani. "Circulating Vasoactive Peptide Urotensin II and Relationships with Cardiovascular Disease." In Biomarkers in Cardiovascular Disease, 1–23. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-007-7741-5_6-1.

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Mallamaci, Francesca, Daniela Leonardis, and Maria Borrajo. "Role of Novel Biomarkers in Chronic Kidney Disease: Urotensin II." In Cardiorenal Syndrome, 299–308. Milano: Springer Milan, 2010. http://dx.doi.org/10.1007/978-88-470-1463-3_23.

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Brkovic, A., P. Lampron, M. Létourneau, and A. Fournier. "Identification of Key-Residues of Urotensin II, a Potent Mammalian Vasoconstrictor." In Peptides: The Wave of the Future, 725–26. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_338.

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Grieco, Paolo, Riccardo Patacchini, Alfonso Carotenuto, Carlo A. Maggi, Ettore Novellino, and Paolo Rovero. "Design, Synthesis and Conformational Analysis of Human Urotensin II (U-II) Analogues with Lactam Bridge." In Peptides: The Wave of the Future, 630–31. Dordrecht: Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-010-0464-0_293.

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6

Konno, Norifumi. "Urotensin II." In Handbook of Hormones, 88—e11–5. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801028-0.00011-8.

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Konno, Norifumi. "Urotensin II." In Handbook of Hormones, 141–43. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820649-2.00038-3.

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LIHRMANN, ISABELLE, HOWARD A. BERN, and HUBERT VAUDRY. "Urotensin II and Urotensin II–Related Peptide." In Handbook of Biologically Active Peptides, 795–803. Elsevier, 2006. http://dx.doi.org/10.1016/b978-012369442-3/50112-4.

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Lihrmann, Isabelle, Hervé Tostivint, Howard Bern, and Hubert Vaudry. "Urotensin II Peptides." In Handbook of Biologically Active Peptides, 957–65. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-385095-9.00127-5.

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Davenport, Anthony. "Urotensin-II Receptor." In xPharm: The Comprehensive Pharmacology Reference, 1–5. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.60208-9.

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Conference papers on the topic "Urotensin II"

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Merlino, Francesco, Ali M. Yousif, Salvatore Di Maro, Stéphane Turcotte, Julien Dufour-Gallant, David Chatenet, Paolo Santicioli, Ettore Novellino, Paolo Grieco, and William D. Lubell. "Synthesis of N-Methyl and Azasulfuryl Urotensin-II(4-11) Derivatives." In The 24th American Peptide Symposium. Prompt Scientific Publishing, 2015. http://dx.doi.org/10.17952/24aps.2015.184.

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Wang, Dan, Xiangjun Li, and Cai Li. "The effects of urotensin II and its receptor in rat renal interstitial fibrosis." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6029049.

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Grieco, Paolo, Michele Caraglia, Silvia Zappavigna, Francesco Merlino, Ettore Novellino, Amalia Luce, Gaetano Facchini, Luigi Marra, Vincenzo Gigantini, and Renato Franco. "Urotensin-II Receptor Regulates Cell Mobility/Invasion and Determines Prognosis of Bladder Cancer." In The Twenty-Third American and the Sixth International Peptide Symposium. Prompt Scientific Publishing, 2013. http://dx.doi.org/10.17952/23aps.2013.078.

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