scholarly journals The KCa channel as a trigger for the cardioprotection induced by kappa-opioid receptor stimulation - its relationship with protein kinase C

2005 ◽  
Vol 145 (7) ◽  
pp. 984-991 ◽  
Author(s):  
Chun-Mei Cao ◽  
Mai Chen ◽  
Tak-Ming Wong
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Opioid Receptor ◽  
Kappa Opioid Receptor ◽  
Kappa Opioid ◽  
Receptor Stimulation ◽  
Kinase C

scholarly journals Pharmacological and phosphoproteomic approaches to roles of protein kinase C in kappa opioid receptor-mediated effects in mice

2020 ◽  
Vol 181 ◽  
pp. 108324
Author(s):  
Jeffrey J. Liu ◽  
Yi-Ting Chiu ◽  
Chongguang Chen ◽  
Peng Huang ◽  
Matthias Mann ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Opioid Receptor ◽  
Kappa Opioid Receptor ◽  
Kappa Opioid ◽  
Mediated Effects ◽  
Kinase C

scholarly journals Effects of κ-opioid receptor stimulation in the heart and the involvement of protein kinase C

1998 ◽  
Vol 124 (3) ◽  
pp. 600-606 ◽  
Author(s):  
Jin-Song Bian ◽  
Hong-Xin Wang ◽  
Wei-Min Zhang ◽  
Tak-Ming Wong
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Opioid Receptor ◽  
Receptor Stimulation ◽  
Kinase C

scholarly journals Agonist-Dependent And -Independent Kappa Opioid Receptor Phosphorylation Showed Distinct Phosphorylation Patterns And Resulted In Different Cellular Outcomes

2017 ◽  
Author(s):  
Yi-Ting Chiu ◽  
Chongguang Chen ◽  
Stefan Schulz ◽  
Lee-Yuan Liu-Chen
Keyword(s):  
Protein Kinase C ◽  
Opioid Receptor ◽  
Kappa Opioid Receptor ◽  
Kappa Opioid ◽  
Extracellular Signal Regulated Kinase ◽  
Kinase C ◽  
Selective Agonist ◽  
Multiple Protein ◽  
Extracellular Signal ◽  
Pkc Activation

We reported previously that the selective agonist U50,488H promoted phosphorylation of the mouse kappa opioid receptor (KOPR) at residues S356, T357, T363 and S369. Here, we found that agonist (U50,488H)-dependent KOPR phosphorylation at all the residues were mediated by Gi/oα proteins and multiple protein kinases [GRKs2, 3, 5 and 6 and protein kinase C (PKC)]. In addition, PKC activation by phorbol ester induced agonist-independent KOPR phosphorylation. Compared with U50,488H, PKC activation promoted much higher S356/T357 phosphorylation, much lower T363 phosphorylation and similar levels of S369 phosphorylation. Following U50,488H, GRKs, but not PKC, were involved in agonist-induced KOPR internalization. In contrast, PKC activation caused a lower level of agonist-independent KOPR internalization, compared to U50,488H. U50,488H-induced activation of extracellular signal regulated kinase 1/2 (ERK1/2) was G protein-, but not β-arrestin-, dependent. After U50,488H, GRK-mediated, but not PKC-mediated, KOPR phosphorylation followed by β-arrestin recruitment desensitized U50,488H-induced ERK1/2 response. Therefore, agonist-dependent (GRK- and PKC-mediated) and agonist-independent (PKC-promoted) KOPR phosphorylations show distinct phosphorylation patterns, leading to diverse cellular outcomes.

RGSZ1 interacts with protein kinase C interacting protein PKCI-1 and modulates mu opioid receptor signaling

2007 ◽  
Vol 19 (4) ◽  
pp. 723-730 ◽  
Author(s):  
Seena K. Ajit ◽  
Suneela Ramineni ◽  
Wade Edris ◽  
Rachel A. Hunt ◽  
Wah-Tung Hum ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Opioid Receptor ◽  
Mu Opioid Receptor ◽  
Receptor Signaling ◽  
Interacting Protein ◽  
Mu Opioid ◽  
Kinase C

Kappa-opioid peptide receptor stimulation increases cytosolic pH and myofilament responsiveness to Ca2+ in cardiac myocytes

1991 ◽  
Vol 261 (5) ◽  
pp. H1671-H1674 ◽  
Author(s):  
C. Ventura ◽  
M. C. Capogrossi ◽  
H. A. Spurgeon ◽  
E. G. Lakatta
Keyword(s):  
Cardiac Myocytes ◽  
Opioid Receptor ◽  
Kappa Opioid Receptor ◽  
Kappa Opioid ◽  
Methane Sulfonate ◽  
Receptor Stimulation ◽  
Cytosolic Ph ◽  
Prolonged Incubation ◽  
Ventricular Cells ◽  
Stimulation Of

Although kappa- and delta-opioid receptors on mammalian cardiac myocytes have been discovered recently, the intracellular effects that result from stimulation of these receptors remain unknown. We examine the effects of a rapid and brief exposure to a kappa-opioid receptor agonist on intracellular Ca2+, pH, and cell length in individual isolated rat ventricular cells. The specific kappa-agonist trans-dl-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]- benzene-acetamide (U-50488H) (methane sulfonate salt) caused a transient increase in cytosolic pH (pHi) measured from the change in SNARF-1 fluorescence and an increase in cytosolic [Ca2+] (Cai), indexed by a change in indo-1 fluorescence. The initial Cai increase often was followed by Cai oscillations. Both pHi and Cai effects were blocked by the specific antagonist kappa-opioid receptor l-(N-furylmethyl)-alpha-normetazocine methane-sulfonate (Mr 1452). The amplitude of contraction that accompanied the Cai increase elicited by U-50488H was greater than that associated with a similar increase in Cai elicited by electrical stimulation or by the rapid exposure of cells to caffeine. Thus an acute and brief kappa-opioid receptor stimulation of cardiac cells leads to an increase in Cai and pHi. The pHi increase was abolished by 1) blockade of the Na(+)-H+ exchanger by ethyl isopropyl amiloride and 2) inhibition of protein kinase C (PKC) activity via pretreatment with staurosporine or prolonged incubation with 4 beta-phorbol 12-myristate 13-acetate. These maneuvers did not abolish the U-50488H-induced increase in Ca.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscarinic inhibition of ATP-sensitive K+ channels by protein kinase C in urinary bladder smooth muscle

1993 ◽  
Vol 265 (6) ◽  
pp. C1723-C1728 ◽  
Author(s):  
A. D. Bonev ◽  
M. T. Nelson
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Urinary Bladder ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Katp Channels ◽  
Muscle Cells ◽  
Receptor Stimulation ◽  
Kinase C

We explored the possibility that muscarinic receptor stimulation can inhibit ATP-sensitive K+ (KATP) channels in smooth muscle cells from guinea pig urinary bladder. Whole cell K+ currents were measured in smooth muscle cells isolated from the detrusor muscle of the guinea pig bladder. Stimulation of muscarinic receptors by carbachol (CCh; 10 microM) inhibited KATP currents by 60.7%. Guanosine 5'-O-(2-thiodiphosphate) in the pipette (internal) solution prevented the CCh-induced inhibition of KATP currents. Activators of protein kinase C (PKC), a diacylglycerol analogue, and phorbol 12-myristate 13-acetate inhibited KATP currents by 63.5 and 73.9%, respectively. Blockers of PKC (bisindolylmaleimide GF-109203X and calphostin C) greatly reduced CCh inhibition of KATP currents. We propose that muscarinic receptor stimulation inhibits KATP channels in smooth muscle cells from urinary bladder through activation of PKC.

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