Human urotensin II-induced aorta ring contractions are mediated by protein kinase C, tyrosine kinases and Rho-kinase: inhibition by somatostatin receptor antagonists

Rossowski, W; Cheng, Beng-L.; Taylor, John E.; Datta, Rakesh; Coy, David H.

doi:10.1016/s0014-2999(02)01341-9

Cited by 82 publications

(55 citation statements)

References 26 publications

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“…This phenomenon indicates that Ca 2+ sensitization of contractile mechanisms is activated by urotensin II, supporting the findings in previous reports (8,27 2+ sensitization of contractile elements, which is accompanied by the increase in MLC phosphorylation. The Ca 2+ sensitization is considered to be mainly mediated by inhibition of myosin phosphatase activity via the RhoA/ Rho-kinase system and / or the PKC/ CPI-17 system (14, 28).…”

Section: +supporting

confidence: 92%

“…-channel blockers, verapamil and nitrendipine, can partially inhibit the urotensin II-induced contraction (27) ] i remaining in the presence of verapamil and La 3+ was completely inhibited by thapsigargin, suggesting that Ca 2+ release from sarcoplasmic reticulum is induced by urotensin II. In biochemical analysis, in fact, urotensin II has been shown to stimulate phosphoinositide hydrolysis (7).…”

Section: +mentioning

confidence: 95%

“…Sauzeau et al reported that urotensin II induced vasoconstriction and cell proliferation through the RhoA / Rho-kinase system (8). Rossowski et al (27) indicated that not only Rho-kinase but also PKC regulates urotensin II-induced contraction in rat aorta. In the present study, as shown in Fig.…”

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confidence: 99%

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Mechanism of Human Urotensin II-Induced Contraction in Rat Aorta

et al. 2004

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Abstract. Urotensin II induced sustained contraction with an EC 50 value of 2.29 ± 0.12 nM in rat aorta. Urotensin II (100 nM ] i with only partial inhibition of the contraction elicited by urotensin II. Urotensin II increased myosin light chain (MLC) phosphorylation to a level greater than that induced by 72.7 mM KCl (high K + ). Pretreatment with Go6983 (PKC inhibitor), U0126 (MEK inhibitor), or SB203580 (p38MARK inhibitor) partially inhibited the urotensin II-induced contraction with no effects on the high K + -induced contractions. Wortmannin (MLC kinase inhibitor) only partially inhibited urotensin II-induced contraction, although it completely inhibited the high K + -induced contraction. These results suggest that urotensin II-induced contraction is mediated by the Ca 2+ / calmodulin / MLC kinase system and modulated by the Ca 2+ sensitization mechanisms to increase MLC phosphorylation. In addition, activations of PKC, p38MAPK, and ERK1/ 2 modulate the contractility mediated by urotensin II in rat aorta.

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confidence: 92%

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confidence: 95%

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Mechanism of Human Urotensin II-Induced Contraction in Rat Aorta

et al. 2004

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“…Second, we provided the first evidence that sst 2a receptor protein is localized on ghrelin-positive X/A-like cells of the rat oxyntic mucosa. Third, iv injection of the selective sst 2 agonist S-346-011 (IC 50 7.5-20 nM) (26) induced a rapid decrease in fasting acyl ghrelin levels as well as reduced the Fig. 3.…”

Section: Discussionmentioning

confidence: 99%

“…Blood was withdrawn at 0.5 and 1 h after the end of the procedure and processed for acyl and total ghrelin measurement. The dose of the sst2 antagonist was based on our previous functional studies in rats injected with the sst2 antagonist PRL-2903 (35) and adjusted for the 10-times higher binding affinity of S-406-028 than PRL-2903 to the sst2 receptor (11,50).…”

Section: Experimental Protocolsmentioning

confidence: 99%

Abdominal surgery inhibits circulating acyl ghrelin and ghrelin-O-acyltransferase levels in rats: role of the somatostatin receptor subtype 2

Stengel

Goebel-Stengel

Wang

et al. 2011

American Journal of Physiology-Gastrointestinal and Liver Physi

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NWG, Rivier J, Taché Y. Abdominal surgery inhibits circulating acyl ghrelin and ghrelin-O-acyltransferase levels in rats: role of the somatostatin receptor subtype 2. Am J Physiol Gastrointest Liver Physiol 301: G239 -G248, 2011. First published June 2, 2011; doi:10.1152/ajpgi.00018.2011.-Clinical studies are evaluating the efficacy of synthetic ghrelin agonists in postoperative ileus management. However, the control of ghrelin secretion under conditions of postoperative gastric ileus is largely unknown. Peripheral somatostatin inhibits ghrelin secretion in animals and humans. We investigated the time course of ghrelin changes postsurgery in fasted rats and whether somatostatin receptor subtype 2 (sst2) signaling is involved. Abdominal surgery (laparotomy and 1-min cecal palpation) induced a rapid and long-lasting decrease in plasma acyl ghrelin levels as shown by the 64, 67, and 59% reduction at 0.5, 2, and 5 h postsurgery, respectively, compared with sham (anesthesia alone for 10 min, P Ͻ 0.05). Levels were partly recovered at 7 h and fully restored at 24 h. The percentage of acyl ghrelin reduction was significantly higher than that of desacyl ghrelin at 2 h postsurgery and not at any other time point. This was associated with a 48 and 23% decrease in gastric and plasma ghrelin-O-acyltransferase protein concentrations, respectively (P Ͻ 0.001). Ghrelin-positive cells in the oxyntic mucosa expressed sst2a receptor and the sst2 agonist S-346-011 inhibited fasting acyl ghrelin levels by 64 and 77% at 0.5 and 2 h, respectively. The sst2 antagonist S-406-028 prevented the abdominal surgery-induced decreased circulating acyl ghrelin but not the delayed gastric emptying assessed 0.5 h postinjection. These data show that activation of sst2 receptor located on gastric X/A-like cells plays a key role in the rapid inhibition of circulating acyl ghrelin induced by abdominal surgery while not being primarily involved in the early phase of postoperative gastric ileus. gastric emptying; somatostatin receptor 2 agonist; somatostatin receptor 2 antagonist; X/A-like cell POSTOPERATIVE GASTRIC ILEUS is a condition that develops as a consequence of surgery and is associated with delayed gastric emptying and intestinal transit (41). Since prolonged postoperative ileus (POI) is an iatrogenic condition leading to prolonged hospitalization resulting in increased health care costs, the development of effective management strategies to prevent POI is clinically important (74). Recently, the food intake stimulating and gastroprokinetic effects of the peptide hormone ghrelin is gaining recognition for the treatment of POI (9). The long-acting synthetic agonist Tranzyme Pharma-101 was reported to accelerate the recovery of the upper and lower gastrointestinal tract in patients undergoing major abdominal surgery (47), consistent with preclinical evidence that peripheral administration of ghrelin agonists reversed the abdominal surgery-induced delayed gastric emptying in rats and dogs (69). However, the regulation of ghrelin under condition...

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RGS2 Regulates Urotensin II‐Induced Intracellular Ca²⁺ Elevation and Contraction in Glomerular Mesangial Cells

Adebiyi

2013

Journal Cellular Physiology

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Urotensin II (UII), a vasoactive peptide modulates renal hemodynamics. However, the physiological functions of UII in glomerular cells are unclear. In particular, whether UII alters mesangial tone remains largely unknown. The present study investigates the physiological effects of UII on glomerular mesangial cells (GMCs). This study also tested the hypothesis that the regulator of G-protein signaling (RGS) controls UII receptor (UTR) activity in GMCs. RT-PCR, Western immunoblotting, and immunofluorescence revealed UTR expression in cultured murine GMCs. Mouse UII (mUII) stimulated Ca(2+) release from intracellular stores and activated store-operated Ca(2+) entry (SOCE) in the cells. mUII also caused a reduction in planar GMC surface area. mUII-induced [Ca(2+)]i elevation and contraction were attenuated by SB 657510, a UTR antagonist, araguspongin B, an inositol 1,4,5-trisphosphate receptor antagonist, thapsigargin, a sarco/endoplasmic reticulum Ca(2+)-ATPase inhibitor, and La(3+), a store-operated Ca(2+) channel blocker, but not nimodipine, an L-type Ca(2+) channel blocker. In situ proximity ligation assay indicated molecular proximity between endogenous RGS2 and UTR in the cells. Treatment of GMCs with mUII elevated plasma membrane expression of RGS2 by ∼2-fold. mUII also increased the interaction between RGS2 and UTR in the cells. siRNA-mediated knockdown of RGS2 in murine GMCs increased mUII-induced [Ca(2+)]i elevation and contraction by ∼35 and 31%, respectively. These findings indicate that mUII-induced SOCE results in murine GMC contraction. These data also suggest that UTR activation stimulates RGS2 recruitment to GMC plasma membrane as a negative feedback mechanism to regulate UTR signaling.

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Human urotensin II-induced aorta ring contractions are mediated by protein kinase C, tyrosine kinases and Rho-kinase: inhibition by somatostatin receptor antagonists

Cited by 82 publications

References 26 publications

Mechanism of Human Urotensin II-Induced Contraction in Rat Aorta

Mechanism of Human Urotensin II-Induced Contraction in Rat Aorta

Abdominal surgery inhibits circulating acyl ghrelin and ghrelin-O-acyltransferase levels in rats: role of the somatostatin receptor subtype 2

RGS2 Regulates Urotensin II‐Induced Intracellular Ca²⁺ Elevation and Contraction in Glomerular Mesangial Cells

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Human urotensin II-induced aorta ring contractions are mediated by protein kinase C, tyrosine kinases and Rho-kinase: inhibition by somatostatin receptor antagonists

Cited by 82 publications

References 26 publications

Mechanism of Human Urotensin II-Induced Contraction in Rat Aorta

Mechanism of Human Urotensin II-Induced Contraction in Rat Aorta

Abdominal surgery inhibits circulating acyl ghrelin and ghrelin-O-acyltransferase levels in rats: role of the somatostatin receptor subtype 2

RGS2 Regulates Urotensin II‐Induced Intracellular Ca2+ Elevation and Contraction in Glomerular Mesangial Cells

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RGS2 Regulates Urotensin II‐Induced Intracellular Ca²⁺ Elevation and Contraction in Glomerular Mesangial Cells