scholarly journals Role of protein kinase C in constrictor responses of the rat basilar artery in vivo.

1992 ◽  
Vol 445 (1) ◽  
pp. 169-179 ◽  
Author(s):  
M A Murray ◽  
F M Faraci ◽  
D D Heistad
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Basilar Artery ◽  
Kinase C

scholarly journals In vivo evidence for a role of protein kinase C in peripheral nociceptive processing

2002 ◽  
Vol 135 (1) ◽  
pp. 239-247 ◽  
Author(s):  
Adriano L S Souza ◽  
Fabrício A Moreira ◽  
Karine R Almeida ◽  
Caryne M Bertollo ◽  
Karina A Costa ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Kinase C ◽  
Nociceptive Processing

scholarly journals Regulation of Impaired Protein Kinase C Signaling by Chemokines in Murine Macrophages during Visceral Leishmaniasis

2005 ◽  
Vol 73 (12) ◽  
pp. 8334-8344 ◽  
Author(s):  
Ranadhir Dey ◽  
Arup Sarkar ◽  
Nivedita Majumder ◽  
Suchandra Bhattacharyya (Majumdar) ◽  
Kaushik Roychoudhury ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Leishmania Donovani ◽  
Disease Process ◽  
Kinase C ◽  
Parasitic Burden ◽  
Infected Cells

ABSTRACT The protein kinase C (PKC) family regulates macrophage function involved in host defense against infection. In the case of Leishmania donovani infection, the impairment of PKC-mediated signaling is one of the crucial events for the establishment of parasite into the macrophages. Earlier reports established that C-C chemokines mediated protection against leishmaniasis via the generation of nitric oxide after 48 h. In this study, we investigated the role of MIP-1α and MCP-1 in the regulation of impaired PKC activity in the early hours (6 h) of infection. These chemokines restored Ca2+-dependent PKC activity and inhibited Ca2+-independent atypical PKC activity in L. donovani-infected macrophages under both in vivo and in vitro conditions. Pretreatment of macrophages with chemokines induced superoxide anion generation by activating NADPH oxidase components in infected cells. Chemokine administration in vitro induced the migration of infected macrophages and triggered the production of reactive oxygen species. In vivo treatment with chemokines significantly restricted the parasitic burden in livers as well as in spleens. Collectively, these results indicate a novel regulatory role of C-C chemokines in controlling the intracellular growth and multiplication of L. donovani, thereby demonstrating the antileishmanial properties of C-C chemokines in the disease process.

scholarly journals Phosphorylation of human pleckstrin on Ser-113 and Ser-117 by protein kinase C

1996 ◽  
Vol 314 (3) ◽  
pp. 937-942 ◽  
Author(s):  
Karen L. CRAIG ◽  
Calvin B. HARLEY
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Phosphorylation Sites ◽  
Wild Type ◽  
Cos Cells ◽  
Phospholipid Hydrolysis ◽  
Kinase C

During platelet activation, receptor-coupled phospholipid hydrolysis stimulates protein kinase C (PKC) and results in the phosphorylation of several proteins, the most prominent being pleckstrin. Pleckstrin is composed of two repeated domains, now called pleckstrin homology (PH) domains, separated by a spacer region that contains several consensus PKC phosphorylation sites. To determine the role of PKC-dependent phosphorylation in pleckstrin function, we mapped the phosphorylation sites in vivo of wild-type and site-directed mutants of pleckstrin expressed in COS cells. Phosphorylation was found to occur almost exclusively on Ser-113 and Ser-117 within the sequence 108-KFARKS*TRRS*IRL-120. Phosphorylation of these sites was confirmed by phosphorylation of the corresponding wild-type and mutant synthetic peptides in vitro.

Effect of protein kinase C inhibitors on endothelin- and vasopressin-induced constriction of the rat basilar artery

1992 ◽  
Vol 263 (6) ◽  
pp. H1643-H1649 ◽  
Author(s):  
M. A. Murray ◽  
F. M. Faraci ◽  
D. D. Heistad
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Basilar Artery ◽  
Arginine Vasopressin ◽  
Vessel Diameter ◽  
Pkc Inhibitor ◽  
Cranial Window ◽  
Kinase C ◽  
Basilar Arteries

The goal of this study was to determine whether inhibitors of protein kinase C (PKC) attenuate constrictor responses of the basilar artery in vivo to endothelin and arginine vasopressin. In anesthetized rats, the diameter of basilar arteries was measured through a cranial window [control diameter 218 +/- 3 (SE) microns]. Vessel diameter was measured during topical application of agonists and antagonists. Sphingosine (10(-6) M), a PKC inhibitor that binds to the regulatory site of PKC, attenuated vasoconstriction in response to endothelin (10(-9), 10(-8), and 10(-7) M) and vasopressin (10(-9) and 10(-8) M). H-7 (10(-9) M), a PKC inhibitor that binds to the catalytic site of PKC, also inhibited vasoconstriction in response to endothelin and vasopressin. Sphingosine and H-7 did not affect baseline diameter and did not attenuate vasoconstriction in response to prostaglandin (PG) F2 alpha. The V1 antagonist [d(CH2)5Tyr(Me)]arginine vasopressin (10(-8) M) significantly inhibited constriction in response to vasopressin (10(-9) and 10(-8) M) but not PGF2 alpha (10(-6) M). These observations suggest that activation of PKC may contribute to endothelin-induced constriction of the basilar artery in vivo and that PKC may also be a mediator of V1-receptor-mediated constriction of the basilar artery in response to vasopressin.

scholarly journals Role of Protein Kinase C in the Pathogenesis of Cerebral Vasospasm after Subarachnoid Hemorrhage

1993 ◽  
Vol 13 (2) ◽  
pp. 247-254 ◽  
Author(s):  
Masaharu Sako ◽  
Jun Nishihara ◽  
Shinsuke Ohta ◽  
Jinze Wang ◽  
Saburo Sakaki
Keyword(s):  
Protein Kinase C ◽  
Subarachnoid Hemorrhage ◽  
Protein Kinase ◽  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Sustained Contraction ◽  
Kinase C ◽  
Intracisternal Injection ◽  
Membrane Bound

This study investigated the role of protein kinase C (PKC) in the pathogenesis of vasospasm after experimental subarachnoid hemorrhage (SAH). PKC activation by intracisternal injection of a phorbol ester [12- O-tetradecanoylphorbol-13-acetate (TP)] induced dose-dependent, slowly developing, severe contraction of the basilar artery. A single intracisternal injection of TP (5 × 10−9 M in the CSF) induced sustained contraction lasting over 3 days, which almost paralleled the changes of membrane-bound PKC activity in the basilar arterial wall. In a two-hemorrhage SAH model, membrane-bound PKC activity in the basilar artery increased up to day 4 and returned to the control level by day 14, whereas angiographic contraction reached a maximum on day 7 and still persisted at a moderate level on day 14. Thus, there was a discrepancy between arterial PKC activity and arterial contraction. Multiple intracisternal injections of TP produced 30–40% sustained contraction of the basilar artery lasting for more than 10 days along with sustained activation of PKC to levels compatible with that observed in the SAH model. However, TP injection caused considerably milder histological changes in the basilar artery than those noted in the SAH model. We concluded that cerebral vasospasm after SAH cannot be explained solely on the basis of activation of the PKC pathway.

Evalution of oxidative stress in diabetic animals by in vivo electron spin resonance measurement—role of protein kinase C

2004 ◽  
Vol 66 ◽  
pp. S109-S113 ◽  
Author(s):  
Toshiyo Sonta ◽  
Toyoshi Inoguchi ◽  
Hirotaka Tsubouchi ◽  
Naotaka Sekiguchi ◽  
Kunihisa Kobayashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase C ◽  
Electron Spin Resonance ◽  
Protein Kinase ◽  
Electron Spin ◽  
Electron Spin Resonance Measurement ◽  
Kinase C ◽  
Spin Resonance

CONTROL OF HYALURONAN SECRETION INTO JOINT FLUID IN VIVO: ROLE OF PROTEIN KINASE C (PKC)

Hyaluronan ◽  
2002 ◽  
pp. 369-374 ◽  
Author(s):  
C.L. Anggiansah ◽  
D. Scott ◽  
A. Poli ◽  
P.J. Coleman ◽  
J. James ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Joint Fluid ◽  
Kinase C

scholarly journals Specificity of protein phosphatases in the dephosphorylation of protein kinase C

1986 ◽  
Vol 240 (1) ◽  
pp. 63-67 ◽  
Author(s):  
P J Parker ◽  
J Goris ◽  
W Merlevede
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Relative Role ◽  
Phosphorylation State ◽  
Kinase C ◽  
Weak Activity ◽  
Oligomeric Forms

Protein kinase C can autophosphorylate in vitro and has also been shown to be phosphorylated in vivo. In order to investigate the factors that may determine the phosphorylation state of protein kinase C in vivo, we determined the ability of the ATP + Mg2+-dependent phosphatase and the polycation-stimulated (PCS) phosphatases to dephosphorylate protein kinase C in vitro. These studies show that all the oligomeric forms of the PCS phosphatases (PCSH1, PCSH2, PCSM and PCSL phosphatases) are effective in the dephosphorylation of protein kinase C, showing 34-82% of the activity displayed with phosphorylase a as substrate. In contrast both the catalytic subunit of the PCS phosphatase and that of the ATP+Mg2+-dependent phosphatase showed only weak activity with protein kinase C as substrate. All these phosphatases, however, were activated by protamine (Ka 14-16 micrograms/ml) through what appears to be a substrate-directed effect. The relative role of these phosphatases in the control of protein kinase C is discussed.

The Role of the Adenosine Receptor Subtypes and Protein Kinase C in Ischemic Preconditioning in the in Vivo Cat Heart

1996 ◽  
Vol 26 (5) ◽  
pp. 1038
Author(s):  
Young Jo Kim ◽  
Dong Gu Shin ◽  
Jong Seon Park ◽  
Kyo Won Choi ◽  
Bong Sub Shim
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Ischemic Preconditioning ◽  
Adenosine Receptor ◽  
Receptor Subtypes ◽  
Kinase C ◽  
Cat Heart

The role of active smooth-muscle contraction in the occurrence of chronic vasospasm in the canine two-hemorrhage model

1994 ◽  
Vol 80 (2) ◽  
pp. 276-282 ◽  
Author(s):  
Toru Matsui ◽  
Hiroyuki Kaizu ◽  
Shoichi Iron ◽  
Takao Asano
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Muscle Contraction ◽  
Basilar Artery ◽  
Smooth Muscle Contraction ◽  
Passive Component ◽  
Kinase C ◽  
Chronic Vasospasm

✓ To evaluate the pathogenetic role of alterations in the physical properties of the arterial wall (the passive component) and of active smooth-muscle contraction (the active component) in the occurrence of chronic vasospasm, the temporal profiles of these events were examined using the canine “two-hemorrhage” model. In the in vivo study, the basilar artery was exposed via the transclival approach on Day 0, 2, 4, 7, or 14. Nicardipine, followed by the protein kinase C inhibitor H-7, then papaverine were administered in a cumulative fashion, and the change in the basilar artery diameter induced by the addition of each agent was recorded angiographically. Drug administration markedly reversed the arterial narrowing caused by chronic vasospasm. When the vasodilatory effect of each agent was compared, the dilation induced by nicardipine or papaverine progressively decreased from Day 2 to Day 7, whereas that induced by H-7 increased. The in vitro experiment using arterial segments excised from the basilar artery revealed a progressive increase in arterial stiffness from Day 2 to Day 7. Also, there was a significant decrease in the initial half-circumference of the arterial segment, which was at its maximum on Days 4 and 7. However, the alteration in the initial half-circumference was considerably less than that in the angiographic diameter following subarachnoid hemorrhage. These data indicate that the augmented spontaneous tonus of the smooth muscle plays the predominant role in the occurrence of chronic vasospasm. Thus, the involvement of the protein kinase C-mediated contractile system is strongly suggested.

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