Protein kinase C in uterine and systemic arteries during ovarian cycle and pregnancy

1991 ◽  
Vol 260 (3) ◽  
pp. E464-E470 ◽  
Author(s):  
R. R. Magness ◽  
C. R. Rosenfeld ◽  
B. R. Carr
Keyword(s):  
Blood Flow ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Luteal Phase ◽  
Follicular Phase ◽  
Ovarian Cycle ◽  
Corpora Lutea ◽  
Kinase C ◽  
Estrogen Production ◽  
Systemic Artery

Elevated uterine blood flow is associated with increases in local estrogen-to-progesterone ratios during the follicular phase of the ovarian cycle and late pregnancy. Because protein kinase C (PKC) activation increases arterial tone, decreased PKC activity may mediate vasodilation. Therefore, we determined uterine (UA) and systemic artery (SA, omental) PKC activity (pmol.mg protein-1.min-1) during the follicular (n = 6), early luteal (n = 4), and late luteal (n = 3) phases of the sheep ovarian cycle, and at 110 +/- 3 (n = 4) and 130 +/- 1 (n = 8) (+/- SE) days of ovine gestation. The stage of the ovarian cycle was verified by the presence of follicles (high estrogen) or corpora lutea (high progesterone) on the ovary and by plasma estrogen and progesterone concentrations. UA-PKC activity (pmol.mg protein-1.min-1) during the follicular phase was 100 +/- 18 and increased progressively to 155 +/- 28 during the early luteal phase and to 219 +/- 37 (P less than 0.05) during the late luteal phase; SA-PKC activity was unchanged. A local utero-ovarian relationship was observed, i.e., UA-PKC activity was lower (P less than 0.001) in UA ipsilateral to ovaries with only follicles (105 +/- 14) when compared with UA adjacent to ovaries with corpora lutea (224 +/- 26), which was similar to SA-PKC activity (184 +/- 35). UA-PKC activity fell from 344 +/- 70 at 110 days to 109 +/- 12 at 130 days gestation (P less than 0.05); SA-PKC activity was unchanged. During the ovarian cycle and latter one-third of ovine pregnancy, increased estrogen production is associated with decreased UA-PKC activity; thus local ovarian and placental steroids may alter PKC activity, thereby regulating UA tone and blood flow.

Isoflurane-enhanced Recovery of Canine Stunned Myocardium 

1999 ◽  
Vol 91 (3) ◽  
pp. 713-713 ◽  
Author(s):  
Wolfgang G. Toller ◽  
Matthew W. Montgomery ◽  
Paul S. Pagel ◽  
Douglas A. Hettrick ◽  
David C. Warltier ◽  
...  
Keyword(s):  
Blood Flow ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Enhanced Recovery ◽  
Contractile Function ◽  
Left Ventricular ◽  
Stunned Myocardium ◽  
Rate Pressure Product ◽  
Kinase C ◽  
Rate Of Increase

Background Isoflurane enhances the functional recovery of postischemic, reperfused myocardium by activating adenosine A1 receptors and adenosine triphosphate-regulated potassium channels. Whether protein kinase C is involved in this process is unknown. The authors tested the hypothesis that inhibition of protein kinase C, using the selective antagonist bisindolylmaleimide, attenuates isoflurane-enhanced recovery of stunned myocardium in dogs. Methods Fifty dogs were randomly assigned to receive intracoronary vehicle or bisindolylmaleimide (2 or 8 microg/min) in the presence or absence of isoflurane (1 minimum alveolar concentration). Five brief (5 min) coronary artery occlusions interspersed with 5-min reperfusion periods followed by 180 min of final reperfusion were used to produce myocardial stunning. Hemodynamics, regional segment shortening, and myocardial blood flow (radioactive microspheres) were measured at selected intervals. Results There were no differences in baseline hemodynamics, segment shortening, or coronary collateral blood flow between groups. Isoflurane significantly (P<0.05) decreased heart rate, mean arterial pressure, rate pressure product, and the maximum rate of increase of left ventricular pressure (+dP/dt(max)) in the presence or absence of bisindolylmaleimide. Sustained contractile dysfunction was observed in dogs that received vehicle (recovery of segment shortening to 12+/-8% of baseline), in contrast to those that received isoflurane (75+/-7% recovery). Bisindolylmaleimide at a dose of 2 microg/min alone enhanced recovery of segment shortening (50+/-7% of baseline) compared with vehicle-pretreated dogs, and isoflurane in the presence of 2 microg/min bisindolylmaleimide further enhanced recovery of contractile function (79+/-8% of baseline). In contrast, 8 microg/min bisindolylmaleimide alone (32+/-12%) or combined with isoflurane (37+/-17%) did not enhance recovery of segment shortening compared with vehicle-pretreated dogs. Conclusions The results indicate that protein kinase C inhibition using low doses of bisindolylmaleimide alone produces cardioprotection, and isoflurane further enhances this protection. In contrast, high doses of bisindolylmaleimide are not cardioprotective in the presence or absence of isoflurane. A role for protein kinase C during isoflurane-induced recovery of the stunned myocardium cannot be excluded.

scholarly journals Disturbed flow: p53 SUMOylation in the turnover of endothelial cells

2011 ◽  
Vol 193 (5) ◽  
pp. 805-807 ◽  
Author(s):  
Wakako Takabe ◽  
Noah Alberts-Grill ◽  
Hanjoong Jo
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Protein Inhibitor ◽  
Disturbed Flow ◽  
Antiapoptotic Protein ◽  
Kinase C

Disturbed blood flow induces apoptosis of vascular endothelial cells, which causes atherosclerosis. In this issue, Heo et al. (2011. J. Cell Biol. doi:10.1083/jcb.201010051) sheds light on p53’s role in this phenomenon. Disturbed flow induces peroxynitrite production, which activates protein kinase C ζ and it’s binding to the E3 SUMO (small ubiquitin-like modifier) ligase PIASy (protein inhibitor of activated STATy). This leads to p53 SUMOylation and its export to the cytosol, where it binds to the antiapoptotic protein Bcl-2 to induce apoptosis.

scholarly journals Erratum

1992 ◽  
Vol 12 (4) ◽  
pp. 707-707 ◽  
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Protein Kinase C ◽  
Cerebral Blood Flow ◽  
Protein Kinase ◽  
Vertical Axis ◽  
Smooth Muscle Contraction ◽  
Kinase C ◽  
Chronic Cerebral Vasospasm

Possible Role of Protein Kinase C-Dependent Smooth Muscle Contraction in the Pathogenesis of Chronic Cerebral Vasospasm Tohru Matsui, Yoh Takuwa, Hiroo Johshita, Kamejiro Yamashita, and Takao Asano [Originally published in Journal of Cerebral Blood Flow and Metabolism 1992;11:143–149] On page 147 of the above, the unit on the left vertical axis of Figure 3 was incorrectly shown as “DAG Level (fLmollmg . protein).” The correct unit is “nmollmg protein.” The figure is shown below. The authors regret this error. [Figure: see text]

scholarly journals The role of protein kinase C and PI3-kinase in the mechanism of the cardioprotective effect of remote ischemic postconditioning

2022 ◽  
Vol 20 (4) ◽  
pp. 6-10
Author(s):  
A. V. Mukhomedzyanov ◽  
N. V. Naryzhnaya ◽  
L. N. Maslov
Keyword(s):  
Blood Flow ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Infarct Size ◽  
Coronary Blood Flow ◽  
Pi3 Kinase ◽  
Ischemic Postconditioning ◽  
Kinase C ◽  
Remote Ischemic Postconditioning

Background. Acute myocardial infarction (AMI) with ST segment elevation is associated with high incidence of complications. Mortality from AMI is about 5%, which has not decreased in recent years. Revascularization provides recovery of coronary blood flow, but also contributes to the occurrence of reperfusion injury to the heart. Remote ischemic postconditioning (RIPostC) is a promising, non-invasive method that can effectively and safely reduce the infarct size.The aim of the study was to investigate the role of protein kinase C and PI3-kinase in the development of the infarct-limiting effect of remote ischemic postconditioning.Materials and methods. The study was performed on Wistar rats. Coronary artery occlusion (45 min) and reperfusion (2 h) were performed. The infarct size (IS) and the size of area at risk (AAR) were assessed. RIPostC was modeled by applying tourniquets to the hind limbs in the hip joint immediately after the restoration of coronary blood flow. All inhibitors were administered intravenously 10 min before reperfusion.Results. In the control group, the IS / AAR ratio was 44%. RIPostC reduced the IS / AAR ratio by about 50%. Preliminary administration of the protein kinase C inhibitor chelerythrine and the PI3-kinase inhibitor wortmannin eliminated the cardioprotective effect of RIPostC.Conclusion. The mechanism of the infarct-limiting effect of RIPostC is implemented through activation of protein kinase C and PI3-kinase. 

Effects of the protein kinase Cβ inhibitor LY333531 on neural and vascular function in rats with streptozotocin-induced diabetes

2002 ◽  
Vol 103 (3) ◽  
pp. 311-321 ◽  
Author(s):  
Mary A. COTTER ◽  
Alison M. JACK ◽  
Norman E. CAMERON
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Sciatic Nerve ◽  
Conduction Velocity ◽  
Superior Cervical Ganglion ◽  
Thermal Hyperalgesia ◽  
Kinase C ◽  
Cervical Ganglion

Elevated protein kinase C activity has been linked to the vascular and neural complications of diabetes. The aim of the present study was to examine the involvement of the β-isoform of protein kinase C in abnormalities of neuronal function, neural tissue perfusion and endothelium-dependent vasodilation in diabetes, by treatment with the selective inhibitor LY333531 (10mg·kg-1·day-1). Diabetes was induced in rats by streptozotocin; the duration of diabetes was 8 weeks. Nerve conduction velocity was monitored, and responses to noxious mechanical and thermal stimuli were estimated by the Randall–Sellito and Hargreaves tests respectively. Sciatic nerve and superior cervical ganglion blood flow were measured by microelectrode polarography and hydrogen clearance. Vascular responses were examined using the in vitro mesenteric bed preparation. An 8-week period of diabetes caused deficits in sciatic motor (20%) and saphenous nerve sensory (16%) conduction velocity, which were reversed by LY333531. Diabetic rats had mechanical and thermal hyperalgesia. LY333531 treatment did not affect mechanical thresholds, but corrected thermal hyperalgesia. Sciatic nerve and superior cervical ganglion blood flow were both reduced by 50% by diabetes; this was almost completely corrected by 2 weeks of LY333531 treatment. Diabetes caused a 32% reduction in vasodilation of the mesenteric vascular bed in response to acetylcholine, mediated by nitric oxide and endothelium-derived hyperpolarizing factor. When the former was abolished during nitric oxide synthase inhibition, an 80% diabetic deficit in the remaining relaxation was noted. LY333531 treatment attenuated the development of these defects by 64% and 53% respectively. Thus protein kinase Cβ contributes to the neural and vascular complications of experimental diabetes; LY333531 is a candidate for further study in clinical trials of diabetic neuropathy and vasculopathy.

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