Ischemia-Induced Translocation of Protein Kinase C-.EPSILON. Mediates Cardioprotection in the Streptozotocin-Induced Diabetic Rat

Ooie, Tatsuhiko; Takahashi, Naohiko; Nawata, Tomoko; Arikawa, Masaya; Yamanaka, Kunitoshi; Kajimoto, Munetaka; Shinohara, Tetsuji; Shigematsu, Sakuji; Hara, Masahide; Yoshimatsu, Hironobu; Saikawa, Tetsunori

doi:10.1253/circj.67.955

Cited by 24 publications

(19 citation statements)

References 34 publications

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“…Second, it is still controversial as to whether the STZ-induced diabetic heart is sensitive to or tolerant of ischemic insult (24,25). We reported previously that diabetic hearts, isolated 12 weeks after STZ injection, showed better reperfusion-induced LV functional recovery (26,27). In the present study, the hyperthermia-treated STZ-induced diabetic heart showed poor reperfusion-induced LV functional recovery compared with the hyperthermia-treated control heart.…”

Section: Discussionmentioning

confidence: 46%

“…For instance, myocardial concentrations of creatine phosphate during reperfusion were greater in the 12-week STZinduced diabetic rat heart (28). We also reported that translocation of the protein kinase C ⑀-isoform from the cytosol to particulate during ischemia plays a key role in cardioprotection against ischemia-reperfusion injury in the 12-week STZ-induced diabetic heart (26). Finally, insulin deficiency stimulates lipolysis in adipose tissue, increasing the delivery of free fatty acid from adipose tissue to liver and consequently, triglyceride production in liver.…”

Section: Discussionmentioning

confidence: 75%

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Phosphatidylinositol 3-Kinase–Dependent Activation of Akt, an Essential Signal for Hyperthermia-Induced Heat-Shock Protein 72, Is Attenuated in Streptozotocin-Induced Diabetic Heart

et al. 2006

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We tested the hypothesis that phosphatidylinositol 3-kinase (PI 3-kinase)-dependent activation of Akt is essential for the expression of cardiac heat-shock protein 72 (HSP72) and that this pathway is impaired in the streptozotocin (STZ)-induced diabetic heart. STZ-induced male diabetic rats were treated with insulin (STZ-insulin group, n ‫؍‬ 26) or vehicle (STZ-vehicle group, n ‫؍‬ 61) for 3 weeks. Whole-body hyperthermia (43°C for 20 min) was applied, and the heart was isolated 24 h later. Compared with control heart, hyperthermia-induced HSP72 expression and phosphorylation of Akt were attenuated in the STZvehicle heart. Pretreatment with wortmannin attenuated hyperthermia-induced HSP72 expression and phosphorylation of Akt. In isolated perfused heart experiments, the hyperthermia-treated STZ-vehicle heart showed poor left ventricular functional recovery during reperfusion after no-flow global ischemia compared with hyperthermiatreated control heart. Insulin treatment restored HSP72 expression and reperfusion-induced functional recovery. In cultured neonatal rat cardiomyocytes, hyperthermiainduced HSP72 expression was enhanced by insulin, together with tolerance against hypoxia-reoxygenation injury. Wortmannin and LY294002 inhibited hyperthermia-induced HSP72 expression and phosphorylation of Akt. Our results indicate that activation of Akt, in a PI 3-kinase-dependent manner, is essential for hyperthermia-induced HSP72 expression in association with cardioprotection, suggesting impairment of this signaling pathway in the STZ-induced diabetic heart, probably due to insulin deficiency. Diabetes 55: 1307-1315, 2006 S tudies from our laboratory and those of other investigators have shown that heat-shock protein 72 (HSP72), induced by hyperthermia, protects the heart against ischemia-reperfusion injury (1-3). Streptozotocin (STZ)-induced diabetic rats have been widely used as a model of insulin-deficient diabetes and are known to exhibit various cardiac abnormalities (4). However, the effects of STZ-induced diabetes on HSP72 expression in the heart remain inconclusive. Joyeux et al. (5) reported that, although hyperthermia induced comparable expression levels of HSP72 in normal and diabetic hearts, the size of the infarction induced by coronary artery occlusion followed by reperfusion was larger in the diabetic than in the normal heart. Based on these observations, Joyeux et al. (5) concluded that the myocardial protective effect of hyperthermia did not extend to STZ-induced diabetic rats and seemed to be unrelated to the HSP72 level. Recently, however, Qi et al. (6) reported that preconditioning with a -opioid receptor agonist, U50,488H, increased cardiac HSP72 expression and reduced the infarct size induced by coronary artery occlusion in the normal heart 24 h after preconditioning but not in the STZ-induced diabetic rat heart. They concluded that lack of a U50,488H cardioprotective effect could, at least in part, be due to impaired synthesis of HSP72 in the STZ-induced diabetic heart (6).Activation of Akt prom...

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Section: Discussionmentioning

confidence: 46%

Section: Discussionmentioning

confidence: 75%

Phosphatidylinositol 3-Kinase–Dependent Activation of Akt, an Essential Signal for Hyperthermia-Induced Heat-Shock Protein 72, Is Attenuated in Streptozotocin-Induced Diabetic Heart

et al. 2006

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“…As regards conventional PKCs, the mRNA expression of PKC-α is higher in SHR than WKY aorta, as it is in the heart where it may be related to hypertrophy (Dorn and Force, 2005). The expression of PKC-ε, a novel PKC isoform mediating cardioprotection (Ooie et al, 2003), was greater in SHR than in WKY aortae. This may seem counter-intuitive because the former strain is the one exhibiting cardiovascular dysfunction.…”

Section: Figurementioning

confidence: 92%

α₁‐Adrenoceptor activation of PKC‐ε causes heterologous desensitization of thromboxane receptors in the aorta of spontaneously hypertensive rats

Zhao

Vanhoutte

Leung

2015

British J Pharmacology

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BACKGROUND AND PURPOSEIn the aorta of adult spontaneously hypertensive (SHR), but not in that of normotensive Wistar-Kyoto (WKY), rats, previous exposure to phenylephrine inhibits subsequent contractions to PGE2. The present experiments were designed to examine the mechanism(s) underlying this inhibition. EXPERIMENTAL APPROACHIsometric tension was measured in isolated rings of SHR and WKY aortae. Gene expression and protein presence were measured by quantitative real-time PCR and Western blotting respectively. KEY RESULTSIn aorta of 18 weeks SHR, but not age-matched WKY, pre-exposure to phenylephrine inhibited subsequent contractions to PGE2 that were mediated by thromboxane prostanoid (TP) receptors. This inhibition was not observed in preparations of pre-hypertensive 5-week-old SHR, and was significantly larger in those of 36-than 18-week-old SHR. Pre-exposure to the PKC activator, phorbol 12,13-dibutyrate, also inhibited subsequent contractions to PGE2 in SHR aortae. The selective inhibitor of PKC-ε, ε-V1-2, abolished the desensitization caused by pre-exposure to phenylephrine. Two molecular PKC bands were detected and their relative intensities differed in 36-week-old WKY and SHR vascular smooth muscle. The mRNA expressions of PKC-α, PKC-ε, PK-N2 and PKC-ζ and of G protein-coupled kinase (GRK)-2, GRK4 and β-arrestin2 were higher in SHR than WKY aortae. CONCLUSIONS AND IMPLICATIONSThese experiments suggest that in the SHR but not the WKY aorta, α1-adrenoceptor activation desensitizes TP receptors through activation of PKC-ε. This heterologous desensitization is a consequence of the chronic exposure to high arterial pressure. AbbreviationsPDBu, phorbol 12,13-dibutyrate; SHR, spontaneously hypertensive rat BJP British Journal of Pharmacology

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“…Более того, результаты клинического исследования VALURE (Valsartan Antihypertensive Long -Term Use Evaluation) пока-зали, что среди больных гипертонической болезнью с впервые выявленным СД частота развития ФП достоверно выше, чем среди лиц без нарушений угле-водного обмена [3]. В то же время в литературе суще-ствуют данные о парадоксальных эффектах повыше-ния резистентности к ишемии у животных с модели-рованным СД [4]. Предыдущими нашими работами также было показано, что на ранних стадиях развития коронарной недостаточности индуцирование СД способствует нормализации сократительной актив-ности папиллярных мышц крыс [5].…”

Section: +unclassified

“…Этот факт достаточно хорошо согласуется с результатами других исследований, сви-детельствующих об усилении ишемической резистент-ности миокарда животных с небольшим сроком стреп- тозотоцин-индуцированного диабета [4]. Вполне вероятно, что при сочетанном развитии постинфаркт-ного кардиосклероза и СД в эксперименте совокуп-ность метаболических изменений в ранний период развития патологических состояний приводит к реа-лизации адаптационных возможностей миокарда.…”

Section: +unclassified

MAINTENANCE OF СА2+-ATP-ASE AMOUNT IN SARCOPLASMATIC RETICULUM CARDIOMYOCYTES IN ISCHEMIC MYOCARDIUM DURING SHORT DURATION OF DIABETES MELLITUS COURSE Kondratyeva D. S., Afansyev S. A., Kanev A. F., Kozlov B. N.

Kondratyeva¹,

Afansyev²,

Канев³

et al. 2014

Russ J Cardiol

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Цель. Исследовать уровень Са 2+-АТФ-азы саркоплазматического ретикулума (СР) в миокарде человека при ишемической болезни сердца (ИБС) и при ИБС, ассоциированной с сахарным диабетом (СД) II типа, а также у животных с постинфарктным кардиосклерозом, сочетанным с СД. Материал и методы. Работа выполнена на биопсийном материале сердца пациентов и крыс с хронической ишемией миокарда, сочетанной с СД. Фраг-мент ушка правого предсердия (биопсийный материал) иссекали на стадии подключении аппарата искусственного кровообращения. Постинфарктный кардиосклероз (ПИКС) формировался в течение 6 недель после окклюзии коронарной артерии. СД развивался в течение 6 недель после внутрибрюшин-ной инъекции стрептозотоцина (60 мг/кг MAINTENANCE OF СА 2+ -ATP-ASE AMOUNT IN SARCOPLASMATIC RETICULUM CARDIOMYOCYTES IN ISCHEMIC MYOCARDIUM DURING SHORT DURATION OF DIABETES MELLITUS COURSEKondratyeva D. S., Afansyev S. A., Kanev A. F., Kozlov B. N. Aim. To study the level of Са 2+-ATP-ase of sarcoplasmatic reticulum (SR) in human myocardium in ischemic heart disease (CHD) and in CHD with diabetes mellitus 2nd type (DM), and also in animals with postinfarction cardiosclerosis with DM. Material and methods. The study performed on biopsy material of the hearts from patients and rats with chronic ishemic heart disease wih DM. A piece of left atrial appendage (biopsy material) was cut away during the period of the artificial circulation device setup. Postinfarction cardiosclerosis (PICS) had being formed during 6 weeks after coronary artery occlusion. DM developed during 6 weeks after intraperitoneal injection of streptosotocine (60 mg/kg).

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Ischemia-Induced Translocation of Protein Kinase C-.EPSILON. Mediates Cardioprotection in the Streptozotocin-Induced Diabetic Rat

Cited by 24 publications

References 34 publications

Phosphatidylinositol 3-Kinase–Dependent Activation of Akt, an Essential Signal for Hyperthermia-Induced Heat-Shock Protein 72, Is Attenuated in Streptozotocin-Induced Diabetic Heart

Phosphatidylinositol 3-Kinase–Dependent Activation of Akt, an Essential Signal for Hyperthermia-Induced Heat-Shock Protein 72, Is Attenuated in Streptozotocin-Induced Diabetic Heart

α₁‐Adrenoceptor activation of PKC‐ε causes heterologous desensitization of thromboxane receptors in the aorta of spontaneously hypertensive rats

MAINTENANCE OF СА2+-ATP-ASE AMOUNT IN SARCOPLASMATIC RETICULUM CARDIOMYOCYTES IN ISCHEMIC MYOCARDIUM DURING SHORT DURATION OF DIABETES MELLITUS COURSE Kondratyeva D. S., Afansyev S. A., Kanev A. F., Kozlov B. N.

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Ischemia-Induced Translocation of Protein Kinase C-.EPSILON. Mediates Cardioprotection in the Streptozotocin-Induced Diabetic Rat

Cited by 24 publications

References 34 publications

Phosphatidylinositol 3-Kinase–Dependent Activation of Akt, an Essential Signal for Hyperthermia-Induced Heat-Shock Protein 72, Is Attenuated in Streptozotocin-Induced Diabetic Heart

Phosphatidylinositol 3-Kinase–Dependent Activation of Akt, an Essential Signal for Hyperthermia-Induced Heat-Shock Protein 72, Is Attenuated in Streptozotocin-Induced Diabetic Heart

α1‐Adrenoceptor activation of PKC‐ε causes heterologous desensitization of thromboxane receptors in the aorta of spontaneously hypertensive rats

MAINTENANCE OF СА2+-ATP-ASE AMOUNT IN SARCOPLASMATIC RETICULUM CARDIOMYOCYTES IN ISCHEMIC MYOCARDIUM DURING SHORT DURATION OF DIABETES MELLITUS COURSE Kondratyeva D. S., Afansyev S. A., Kanev A. F., Kozlov B. N.

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α₁‐Adrenoceptor activation of PKC‐ε causes heterologous desensitization of thromboxane receptors in the aorta of spontaneously hypertensive rats