Urocortin 2 induces tyrosine hydroxylase phosphorylation in PC12 cells

Nemoto, Tetsuo; Mano-Otagiri, Asuka; Shibasaki, Tamotsu

doi:10.1016/j.bbrc.2005.03.031

Cited by 20 publications

(22 citation statements)

References 53 publications

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“…In vitro data suggest that UCN2 may regulate catecholamine synthesis and release in the adrenal medulla. In cultured PC12 cells, UCN2 induces norepinephrine release and phosphorylation of tyrosine hydroxylase through protein kinase A and protein kinase A-Erk1/2 pathways respectively (Nemoto et al 2005). However, conversely, UCN2 activation of CRFR2 actually suppresses the secretion of catecholamines in dispersed rat and human adrenal chromaffin cells, whereas UCN1/CRF activation of CRFR1 induces catecholamine secretion (Dermitzaki et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Urocortin 2 induces potent long-lasting inhibition of cardiac sympathetic drive despite baroreflex activation in conscious sheep

Charles

Jardine²,

Rademaker³

et al. 2009

Journal of Endocrinology

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Emerging evidence suggests that the urocortin (UCN) peptides contribute to pressure and volume regulation with possible involvement in the pathophysiology of cardiovascular disease. We have recently reported that i.v. UCN1 potently inhibits cardiac sympathetic nerve activity (CSNA) in normal sheep. However, little is known about possible interactions between UCN2 and the sympathetic nervous system. Accordingly, we have examined the effects of i.v. UCN2 on CSNA, hemodynamics, and plasma catecholamines in normal conscious sheep. Bolus i.v. administration of UCN2 (25 and 100 mg) resulted in the expected hemodynamic actions including transient falls in arterial pressure (PZ0 . 016) and more sustained rises in heart rate (P!0 . 001) and cardiac output (P!0 . 001) and falls in peripheral resistance (P!0 . 001). CSNA burst frequency showed a biphasic response (P!0 . 001) with an acute rise followed by a more prolonged fall. CSNA burst area and incidence showed prolonged, dose-dependent falls in response to UCN2 administration (all P!0 . 001). UCN2 also induced a short-lived rise in plasma norepinephrine levels (PZ0 . 006).The marked rise in heart rate in response to UCN2 is preserved in sheep undergoing pharmacological ganglionic blockade with hexamethonium. In conclusion, this is the first study to report the effects of UCN2 on SNA and indicates potent inhibition of sympathetic traffic to the heart despite a generalized baroreceptor-induced activation of sympathetic activity. These findings suggest an important role for UCN2 in cardiovascular homeostasis and warrant further investigation for potential therapeutic applications in acute myocardial injury and heart disease.

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Section: Discussionmentioning

confidence: 99%

Urocortin 2 induces potent long-lasting inhibition of cardiac sympathetic drive despite baroreflex activation in conscious sheep

Charles

Jardine²,

Rademaker³

et al. 2009

Journal of Endocrinology

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“…Importantly, also estrogenic pollutants ( Yanagihara et al 2005) and phytoestrogens ( Yanagihara et al 2008) have been shown to stimulate or block catecholamine synthesis via ERKs depending on their respective concentration. A number of additional growth factors, like epidermal growth factor (EGF; , Ho et al 2005, insulin (Sugano et al 2006), vasoactive intestinal peptide (VIP; Whitworth et al 2002) and urocortin-2 ( Nemoto et al 2005) were found to affect ERK activation in different medullary cell systems. In addition to the aforementioned growth factors also pharmaceutical agents such as milnacipran (Shinkai et al 2007), chemical factors such as histamine , and nicotine (Cox et al 1996), or even environmental pollutants such as cadmium (Leal et al 2007) impact on medullary ERK activation and in part also catecholamine secretion.…”

Section: Effectors Of Erk1/2 Activation In Adrenocortical Cellsmentioning

confidence: 99%

Mechanisms of adrenal gland growth: signal integration by extracellular signal regulated kinases1/2

Hoeflich¹,

Bielohuby²

2008

Journal of Molecular Endocrinology

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The adrenal gland influences a multitude of processes during stress response, but also potently affects the immune system, glucose metabolism, electrolyte or water homeostasis, and cardiovascular functions. According to the present understanding, the adrenal cortex is tightly controlled by the hypothalamic-pituitary-adrenal axis. This axis involves hypothalamic CRH and pituitary ACTH which determine processes of adrenocortical growth and function. However, control of the adrenal gland comprises a plethora of additional endogenous or exogenous factors. Among those are diverse hormones, psychosocial parameters, physiological stress, secondary plant products, or even environmental pollutants. In the present review, we summarize the current view of endocrine growth control in the adrenal gland. We then discuss intracellular mechanisms of adrenal growth control and focus on extracellular signal regulated kinases 1/2 ( ERK1/2), which have been demonstrated to be controlled by not only ACTH or angiotensin II, but also by a large number of additional effectors. On the basis of these multiple exogenous or endogenous factors which impact on the adrenal gland through ERK1/2 activity, we speculate on a mechanism by which ERK1/2 act as a central integrative growth regulatory elements in the adrenal gland.

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“…Ucn 1 and Ucn 3, as well as CRF receptors, are observed in non-pathological adrenal glands, but at reduced levels in tumor cells of pheochromocytomas, adrenocortical adenomas and carcinomas [90,266], suggesting physiologic relevance or regulation of their expression. Ucn 2 may regulate catecholamine synthesis and release in the adrenal medulla, as, in PC12 cells, it induces noradrenaline release and phosporylation of tyrosine hydroxylase through protein kinase A and protein kinase A-Erk1/2 pathways, respectively [190].…”

Section: Physiologic and Behavioral Effects Of Ucnsmentioning

confidence: 99%

Physiology, pharmacology, and therapeutic relevance of urocortins in mammals: Ancient CRF paralogs

Fekete

Zorrilla

2007

Frontiers in Neuroendocrinology

221

252

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Urocortins, three paralogs of the stress-related peptide corticotropin-releasing factor (CRF) found in bony fish, amphibians, birds and mammals, have unique phylogenies, pharmacologies, and tissue distributions. As a result and despite a structural family resemblance, the natural functions of urocortins and CRF in mammalian homeostatic responses differ substantially. Endogenous urocortins are neither simply counterpoints nor mimics of endogenous CRF action. In their own right, urocortins may be clinically relevant molecules in the pathogenesis or management of many conditions, including congestive heart failure, hypertension, gastrointestinal and inflammatory disorders (irritable bowel syndrome, active gastritis, gastroparesis, rheumatoid arthritis), atopic/ allergic disorders (dermatitis, urticaria, asthma), pregnancy and parturition (preeclampsia, spontaneous abortion, onset and maintenance of effective labor), major depression and obesity. Safety trials for intravenous urocortin treatment have already begun for the treatment of congestive heart failure. Further understanding the unique functions of urocortin 1, urocortin 2 and urocortin 3 action may uncover other therapeutic opportunities. KeywordsUrocortin 1 or urocortin 2 or urocortin 3 or stresscopin or stresscopin-related peptide; corticotropinreleasing factor or CRF or corticotropin-releasing hormone or CRH or corticoliberin; stress response; peptide; anxiety or depression; pregnancy; labor or parturitition; food intake or energy balance or obesity; inflammation or immune system; salt or fluid balance; cardiovascular or hypertension or heart failure; gastrointestinal motility or irritable bowel syndrome

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Urocortin 2 induces tyrosine hydroxylase phosphorylation in PC12 cells

Cited by 20 publications

References 53 publications

Urocortin 2 induces potent long-lasting inhibition of cardiac sympathetic drive despite baroreflex activation in conscious sheep

Urocortin 2 induces potent long-lasting inhibition of cardiac sympathetic drive despite baroreflex activation in conscious sheep

Mechanisms of adrenal gland growth: signal integration by extracellular signal regulated kinases1/2

Physiology, pharmacology, and therapeutic relevance of urocortins in mammals: Ancient CRF paralogs

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