Interactive Role of Protein Kinase C-δ with Rho-Kinase in the Development of Cerebral Vasospasm in a Canine Two-Hemorrhage Model

2005 ◽  
Vol 42 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Kazuo Obara ◽  
Shigeru Nishizawa ◽  
Masayo Koide ◽  
Kayo Nozawa ◽  
Ayako Mitate ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Cerebral Vasospasm ◽  
Rho Kinase ◽  
Kinase C

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.

scholarly journals The Role of Protein Kinase D in Neurotensin Secretion Mediated by Protein Kinase C-α/-δ and Rho/Rho Kinase

2004 ◽  
Vol 279 (27) ◽  
pp. 28466-28474 ◽  
Author(s):  
Jing Li ◽  
Kathleen L. O'Connor ◽  
Mark R. Hellmich ◽  
George H. Greeley ◽  
Courtney M. Townsend ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Rho Kinase ◽  
Protein Kinase D ◽  
Kinase C

scholarly journals Possible Role of Protein Kinase C-Dependent Smooth Muscle Contraction in the Pathogenesis of Chronic Cerebral Vasospasm

1991 ◽  
Vol 11 (1) ◽  
pp. 143-149 ◽  
Author(s):  
Tohru Matsui ◽  
Yoh Takuwa ◽  
Hiroo Johshita ◽  
Kamejiro Yamashita ◽  
Takao Asano
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Muscle Contraction ◽  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Smooth Muscle Contraction ◽  
Kinase C ◽  
Chronic Vasospasm

In the present study, we investigate the possible role of protein kinase C (PKC)-dependent smooth muscle contraction in cerebral vasospasm following subarachnoid hemorrhage (SAH), employing the beagle “two-hemorrhage” model. The occurrence of chronic vasospasm was angiographically confirmed on day 7 in the basilar artery, which was exposed via the transclival approach. The artery was superfused with aerated Krebs-Henseleit solution containing various agents, and the subsequent changes in the basilar artery diameter were recorded by successive angiography. The preexisting spasm was not ameliorated by local application of neurotransmitter antagonists (atropine, methysergide, phentolamine, and diphenhydramine), calmodulin inhibitors (R24571 and W-7), or a calcium antagonist, nicardipine. However, the application of PKC inhibitors such as H-7 and staurosporine induced significant dilation of the artery. In another experiment, an intrinsic PKC activator, 1,2-diacylglycerol (DAG), in the basilar artery, the CSF, and the cisternal clot of beagles exposed to two hemorrhages was measured on days 1,2,4, 7, and 14 using the DAG kinase method. On days 2, 4, and 7, the DAG content of the basilar artery showed a significant and prolonged increase (150–190% of control), whereas it was unchanged on days 1 and 14. Throughout the experimental period, there was a significant linear correlation between the DAG content and the angiographical diameter of the basilar artery. The above results indicate that SAH leads to an increase in the DAG level within the cerebral artery through an as yet unknown mechanism and that subsequent activation of the PKC-dependent contractile system participates in the occurrence of chronic vasospasm.

Role of protein kinase C in the regulation of steroidogenesis in the mouse Leydig cell

1986 ◽  
Vol 113 (1_Suppl) ◽  
pp. S63-S64
Author(s):  
A. K. MUKHOPADHYAY ◽  
H. G. BOHNET
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Leydig Cell ◽  
Kinase C ◽  
Mouse Leydig Cell

scholarly journals Dysregulation of protein kinase C in adult depression and suicide: evidence from postmortem brain studies

2021 ◽  
Author(s):  
Ghanshyam N Pandey ◽  
Anuradha Sharma ◽  
Hooriyah S Rizavi ◽  
Xinguo Ren
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Protein Expression ◽  
Mrna Expression ◽  
Postmortem Brain ◽  
Cortical Region ◽  
Cytosol Fraction ◽  
Kinase C ◽  
Pkc Isozymes

Abstract Background Several lines of evidence suggest the abnormalities of protein kinase C (PKC) signaling system in mood disorders and suicide based primarily on the studies of PKC and its isozymes in the platelets and postmortem brain of depressed and suicidal subjects. In this study we examined the role of PKC isozymes in depression and suicide. Methods We determined the protein and mRNA expression of various PKC isozymes in the prefrontal cortical region [Brodmann area 9 (BA9)] in 24 normal control (NC) subjects, 24 depressed suicide (DS) subjects and 12 depressed non-suicide (DNS) subjects. The levels of mRNA in the prefrontal cortex (PFC) were determined by qRT-PCR and the protein expression was determined by Western blotting. Results We observed a significant decrease in mRNA expression of PKCα, PKCβI, PKCδ and PKCε and decreased protein expression either in the membrane or the cytosol fraction of PKC isozymes - PKCα, PKCβI, PKCβII and PKCδ in DS and DNS subjects compared with NC subjects. Conclusions The current study provides detailed evidence of specific dysregulation of certain PKC isozymes in the postmortem brain of DS and DNS subjects and further supports earlier evidence for the role of PKC in the platelets and brain of adult and teenage depressed and suicidal population. This comprehensive study may lead to further knowledge of the involvement of PKC in the pathophysiology of depression and suicide.

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