Desflurane‐induced and ischaemic postconditioning against myocardial infarction are mediated by <scp>P</scp>im‐1 kinase

Stumpner, Jan; Smul, Thorsten M.; Redel, Andreas; Hilz, T.; Tischer-Zeitz, Tobias; Eisenbarth, Hedwig; Schick, Martin Alexander; Kehl, Franz; Roewer, Norbert; Lange, Markus

doi:10.1111/j.1399-6576.2012.02657.x

Cited by 9 publications

(7 citation statements)

References 43 publications

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“…Kidneys were harvested at the end of the experiment for histopathological studies. Organ tissues were fixed in formaldehyde 3.5% (Otto Fischar, Germany) for more than 24 h. Tissues were stained with haematoxylin and eosin reagent and PAS-reaction as previously described [ 8 , 13 ]. The morphological alterations of kidneys were analysed semi-quantitatively by a blinded investigator where 0 was given when no alterations were found, 1 for mild alterations, 2 for medium alterations and 3 for severe alterations.…”

Section: Methodsmentioning

confidence: 99%

Balanced Hydroxyethylstarch (HES 130/0.4) Impairs Kidney Function In-Vivo without Inflammation

et al. 2015

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Volume therapy is a standard procedure in daily perioperative care, and there is an ongoing discussion about the benefits of colloid resuscitation with hydroxyethylstarch (HES). In sepsis HES should be avoided due to a higher risk for acute kidney injury (AKI). Results of the usage of HES in patients without sepsis are controversial. Therefore we conducted an animal study to evaluate the impact of 6% HES 130/0.4 on kidney integrity with sepsis or under healthy conditions Sepsis was induced by standardized Colon Ascendens Stent Peritonitis (sCASP). sCASP-group as well as control group (C) remained untreated for 24 h. After 18 h sCASP+HES group (sCASP+VOL) and control+HES (C+VOL) received 50 ml/KG balanced 6% HES (VOL) 130/0.4 over 6h. After 24h kidney function was measured via Inulin- and PAH-Clearance in re-anesthetized rats, and serum urea, creatinine (crea), cystatin C and Neutrophil gelatinase-associated lipocalin (NGAL) as well as histopathology were analysed. In vitro human proximal tubule cells (PTC) were cultured +/- lipopolysaccharid (LPS) and with 0.1–4.0% VOL. Cell viability was measured with XTT-, cell toxicity with LDH-test. sCASP induced severe septic AKI demonstrated divergent results regarding renal function by clearance or creatinine measure focusing on VOL. Soleley HES (C+VOL) deteriorated renal function without sCASP. Histopathology revealed significantly derangements in all HES groups compared to control. In vitro LPS did not worsen the HES induced reduction of cell viability in PTC cells. For the first time, we demonstrated, that application of 50 ml/KG 6% HES 130/0.4 over 6 hours induced AKI without inflammation in vivo. Severity of sCASP induced septic AKI might be no longer susceptible to the way of volume expansion.

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Section: Methodsmentioning

confidence: 99%

Balanced Hydroxyethylstarch (HES 130/0.4) Impairs Kidney Function In-Vivo without Inflammation

et al. 2015

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“…Its expression is high in cardiac progenitor cells as it can promote cell proliferation. At the same time, it can act as a downstream molecule of AKT and phosphorylate Bad 112 serine, thus regulating the adaptability of myocardial ischemia injury and increasing myocardial cell survival (Iwakura et al, ; Stumpner et al, ; Hu et al, ; Samse et al, ). Pim‐1 mRNA expression is low in the normal rat cerebellum, brainstem, cerebral cortex, and hippocampus, but high in the pituitary gland.…”

Section: Discussionmentioning

confidence: 99%

Pim‐1 Expression in Rat Retina and its Changes after Optic Nerve Crush

Zhang

Wang

Huang

et al. 2018

The Anatomical Record

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Pim‐1 is a proto‐oncogene which has been discovered to involve in cell proliferation, differentiation, and survival. In this study, we observed the expression of Pim‐1 in neonatal and adult rat retina and the changes in rat retina following optic nerve crush (ONC) in order to explore the relationship between Pim‐1 and the survival of retinal ganglion cells (RGC). We discovered that Pim‐1 was distributed mainly in retinal pigment epithelial cells (RPE) and retinal ganglion cell layer (GCL) in normal newborn rats, and it appeared in RPE, cone rod cell layer and GCL in normal adult rats by immunohistochemistry. Our double immunofluorescent staining of Pim‐1 and γ‐synuclein further confirmed that Pim‐1 was localized in 80% of RGC. Moreover, we found that the amount of Pim‐1 mRNA and protein in adult rat retina was transiently increased after ONC and then decreased 2 weeks after ONC, and the expression level was lower than that of neonatal rat retina under all conditions. We also discovered that Pim‐1 expression in GCL detected by immunohistochemistry was upregulated at Day 1 and Day 3 after ONC, but downregulated at Day 14 after ONC when the survival of RGC was decreased and the apoptotic cells in GCL were increased by hematoxylin‐eosin staining, immunohistochemistry, and TUNEL detection. We suggest that the overexpression of Pim‐1 in the RGC is related to the optic nerve repair while the low expression of Pim‐1 in RGC may be associated with apoptosis and weak intrinsic regeneration ability of RGC. Anat Rec, 301:1968–1976, 2018. © 2018 Wiley Periodicals, Inc.

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“…In mouse heart in vivo, phosphorylation of the pro-apoptotic molecule Bcl-2-associated death (Bad), mediates desflurane-induced PostC via the Pim-1 kinase activation. 16 Pim-1 kinase, a proto-oncogene serine/threonine-protein kinase, was recently identified as a downstream mediator of protein Akt activity in cardiomyocytes: it reduces myocardial infarct size and cardiomyocyte apoptosis and phosphorylates several downstream targets, including Bad. The isolated perfused rat hearts exposed to sevoflurane, in early reperfusion, showed that the expression of Bcl-2 and phospho-Bad increased, and the expression of Bcl-2-associated X protein (Bax: a pro-apoptotic protein) decreased.…”

Section: Impact Of Desflurane and Sevoflurane Post-conditioning On Camentioning

confidence: 99%

The mechanisms of cardio-protective effects of desflurane and sevoflurane at the time of reperfusion: anaesthetic post-conditioning potentially translatable to humans?

Lemoine

Tritapepe

Hanouz

et al. 2016

British Journal of Anaesthesia

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Myocardial conditioning is actually an essential strategy in the management of ischaemia-reperfusion injury. The concept of anaesthetic post-conditioning is intriguing, its action occurring at a pivotal moment (that of reperfusion when ischaemia reperfusion lesions are initiated) where the activation of these cardio-protective mechanisms could overpower the mechanisms leading to ischaemia reperfusion injuries. Desflurane and sevoflurane are volatile anaesthetics frequently used during cardiac surgery. This review focuses on the efficacy of desflurane and sevoflurane administered during early reperfusion as a potential cardio-protective strategy. In the context of experimental studies in animal models and in human atrial tissues in vitro, the mechanisms underlying the cardio-protective effect of these agents and their capacity to induce post-conditioning have been reviewed in detail, underlining the role of reactive oxygen species generation, the activation of the cellular signalling pathways, and the actions on mitochondria along with the translatable actions in humans; this might well be sufficient to set the basis for launching randomized clinical studies, actually needed to confirm this strategy as one of real impact.

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Desflurane‐induced and ischaemic postconditioning against myocardial infarction are mediated by Pim‐1 kinase

Cited by 9 publications

References 43 publications

Balanced Hydroxyethylstarch (HES 130/0.4) Impairs Kidney Function In-Vivo without Inflammation

Balanced Hydroxyethylstarch (HES 130/0.4) Impairs Kidney Function In-Vivo without Inflammation

Pim‐1 Expression in Rat Retina and its Changes after Optic Nerve Crush

The mechanisms of cardio-protective effects of desflurane and sevoflurane at the time of reperfusion: anaesthetic post-conditioning potentially translatable to humans?

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