Different influences of hyperglycemic duration on phosphorylated extracellular signal-regulated kinase 1/2 in rat heart

Naito, Zenya; Takashi, En; Xu, Guang; Ishiwata, Toshiyuki; Teduka, Kiyoshi; Yokoyama, Munehiro; Yamada, Nokutaka; Sugisaki, Yuichi; Asano, Gorō

doi:10.1016/s0014-4800(03)80005-9

Cited by 25 publications

(12 citation statements)

References 47 publications

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“…Differences in animal models, timing and dose of EPO, and more importantly the duration of HG should be attributable to the different results observed in the DM model compared to the current study. Generally, longer duration of DM or HG more significantly repressed organ protective pathways and mitigated protective effects of pharmacologic conditioning in vivo and in vitro experiment (Kobayashi et al, 2007;Naito et al, 2003). Yet, considering the frequent occurrence of transient moderate degree of HG in acute disease states and perioperative period, and the raised concerns regarding its adverse influence on the patients' outcome regardless of the presence of DM (Capes et al, 2000;Ceriello, 2005), the results of the current study should be of significant clinical relevance.…”

Section: Discussionmentioning

confidence: 78%

Erythropoietin protects myocardium against ischemia–reperfusion injury under moderate hyperglycemia

Jun

Jun²,

Shim

et al. 2014

European Journal of Pharmacology

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Section: Discussionmentioning

confidence: 78%

Erythropoietin protects myocardium against ischemia–reperfusion injury under moderate hyperglycemia

Jun

Jun²,

Shim

et al. 2014

European Journal of Pharmacology

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“…However, data are controversial, as increases and decreases have been reported in ERK phosphorylation in STZ models depending on tissue and time. For instance, ERK-1/2 phosphorylation is increased in the kidneys [25], [26] and also in the hearts [27] of rats 4 weeks after the treatment with STZ. In contrast, other authors report a decrease in ERK phosphorylation in heart and white gastrocnemius muscle in rats two weeks after STZ injection [28].…”

Section: Discussionmentioning

confidence: 98%

Tungstate Reduces the Expression of Gluconeogenic Enzymes in STZ Rats

et al. 2012

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AimsOral administration of sodium tungstate has shown hyperglycemia-reducing activity in several animal models of diabetes. We present new insights into the mechanism of action of tungstate.MethodsWe studied protein expression and phosphorylation in the liver of STZ rats, a type I diabetes model, treated with sodium tungstate in the drinking water (2 mg/ml) and in primary cultured-hepatocytes, through Western blot and Real Time PCR analysis.ResultsTungstate treatment reduces the expression of gluconeogenic enzymes (PEPCK, G6Pase, and FBPase) and also regulates transcription factors accountable for the control of hepatic metabolism (c-jun, c-fos and PGC1α). Moreover, ERK, p90rsk and GSK3, upstream kinases regulating the expression of c-jun and c-fos, are phosphorylated in response to tungstate. Interestingly, PKB/Akt phosphorylation is not altered by the treatment. Several of these observations were reproduced in isolated rat hepatocytes cultured in the absence of insulin, thereby indicating that those effects of tungstate are insulin-independent.ConclusionsHere we show that treatment with tungstate restores the phosphorylation state of various signaling proteins and changes the expression pattern of metabolic enzymes.

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“…Hyperglycaemia leads to activation (phosphorylation) of mitogen-activated protein kinases (MAPKs) p38, JNK and ERK1/2, hypertrophy and fibrosis in the heart [32][33][34][35][36][37][38] and kidney [39,40]. While little evidence is available to suggest strong tissue specific activation of proinflammatory pathways in STZ-induced diabetes, pharmacological inhibition or genetic deletion of any of these three MAPKs reduces microvascular complications (diabetic nephropathy, cardiomyopathy and retinopathy) caused by type 1 diabetes in rodents [41,42].…”

Section: Discussionmentioning

confidence: 99%

Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes

et al. 2017

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Aims/hypothesis Microvascular complications in the heart and kidney are strongly associated with an overall rise in inflammation. Annexin A1 (ANXA1) is an endogenous anti-inflammatory molecule that limits and resolves inflammation. In this study, we have used a bedside to bench approach to investigate: (1) ANXA1 levels in individuals with type 1 diabetes; (2) the role of endogenous ANXA1 in nephropathy and cardiomyopathy in experimental type 1 diabetes; and (3) whether treatment with human recombinant ANXA1 attenuates nephropathy and cardiomyopathy in a murine model of type 1 diabetes. Methods ANXA1 was measured in plasma from individuals with type 1 diabetes with or without nephropathy and healthy donors. Experimental type 1 diabetes was induced in mice by injection of streptozotocin (STZ; 45 mg/kg i.v. per day for 5 consecutive days) in C57BL/6 or Anxa1 −/− mice. Diabetic mice were treated with human recombinant (hr)ANXA1(1 μg, 100 μl, 50 mmol/l HEPES; 140 mmol/l NaCl; pH 7.4, i.p.) or vehicle (100 μl, 50 mmol/l HEPES; 140 mmol/l NaCl; pH 7.4, i.p.).Results Plasma levels of ANXA1 were elevated in individuals with type 1 diabetes with/without nephropathy compared with healthy individuals (66.0 ± 4.2/64.0 ± 4 ng/ml vs 35.9 ± 2.3 ng/ml; p < 0.05). Compared with diabetic wild-type (WT) mice, diabetic Anxa1 −/− mice exhibited a worse diabetic phenotype and developed more severe cardiac (ejection fraction; 76.1 ± 1.6% vs 49.9 ± 0.9%) and renal dysfunction (proteinuria; 89.3 ± 5.0 μg/ mg vs 113.3 ± 5.5 μg/mg). Mechanistically, compared with nondiabetic WT mice, the degree of the phosphorylation of mitogenactivated protein kinases (MAPKs) p38, c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK) was significantly higher in non-diabetic Anxa1 −/− mice in both the heart and kidney, and was further enhanced after STZ-induced type 1 diabetes. Prophylactic treatment with hrANXA1 (weeks 1-13) attenuated both cardiac (ejection fraction; 54.0 ± 1.6% vs 72.4 ± 1.0%) and renal (proteinuria; 89.3 ± 5.0 μg/mg vs 53.1 ± 3.4 μg/mg) dysfunction associated with STZ-induced diabetes, while therapeutic administration of hrANXA1 (weeks 8-13), after significant cardiac and renal dysfunction had already developed, halted the further functional decline in cardiac and renal function seen in diabetic mice administered vehicle. In addition, administration of hrANXA1 attenuated the increase in phosphorylation of p38, JNK and ERK, and restored phosphorylation of Akt in diabetic mice. Conclusions/interpretationOverall, these results demonstrate that ANXA1 plasma levels are elevated in individuals with Christoph Thiemermann and Egle Solito contributed equally to this work.Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00125-017-4469-y) contains peer-reviewed but unedited supplementary material, which is available to authorised users.

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Different influences of hyperglycemic duration on phosphorylated extracellular signal-regulated kinase 1/2 in rat heart

Cited by 25 publications

References 47 publications

Erythropoietin protects myocardium against ischemia–reperfusion injury under moderate hyperglycemia

Erythropoietin protects myocardium against ischemia–reperfusion injury under moderate hyperglycemia

Tungstate Reduces the Expression of Gluconeogenic Enzymes in STZ Rats

Annexin A1 attenuates microvascular complications through restoration of Akt signalling in a murine model of type 1 diabetes

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