RISK pathway is involved in oxytocin postconditioning in isolated rat heart

Polshekan, Mirali; Jamialahmadi, Kadijeh; Khori, Vahid; Alizadeh, Ali Mohammad; Saeidi, Mohsen; Ghayour‐Mobarhan, Majid; Jand, Yahya; Ghahremani, Mohammad Hossein; Yazdani, Yaghoub

doi:10.1016/j.peptides.2016.10.001

Cited by 16 publications

(36 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This observation is supported by in vivo studies finding reduced ROS production with chronic OXT treatment in a mouse model of ASD (Wang et al, 2018) as well as reduced oxidative stress status in OXT-treated naïve Wistar rats (Honceriu et al, 2016), ischemia-reperfused Sprague-Dawley rats (Faghihi et al, 2012), and naïve zebrafish (Balmus et al, 2017). Candidate downstream enzymes mediating OXT's effects on ROS production include MAPK/ERK1/2, superoxide dismutase (SOD), and glutathione as antioxidant promoting pathways (Deing et al, 2013;Polshekan et al, 2016;Wang et al, 2018). Moreover, NADPH oxidase-mediated production of ROS is observed to be dampened with the addition of OXT, indicating an effect of attenuating prooxidative pathways (Szeto et al, 2008;Rashed et al, 2011).…”

Section: Oxidative and Inflammatory Stressmentioning

confidence: 91%

“…Suggested to support an anti-inflammatory phenotype, but it remains unclear whether the receptor or peptide is more responsible. Szeto et al, 2008;Rashed et al, 2011;Deing et al, 2013;Honceriu et al, 2016;Polshekan et al, 2016;Wang et al, 2018 Inflammation Pushes most inflammatory cells toward an anti-inflammatory phenotype, though a specific mechanism is unknown. Candidates include activity at NF-κβ and RAGE.…”

Section: Cellular Differentiationmentioning

confidence: 99%

See 1 more Smart Citation

Oxytocin Receptor Signaling in Vascular Function and Stroke

McKay

Counts

2020

Front. Neurosci.

View full text Add to dashboard Cite

The oxytocin receptor (OXTR) is a G protein-coupled receptor with a diverse repertoire of intracellular signaling pathways, which are activated in response to binding oxytocin (OXT) and a similar nonapeptide, vasopressin. This review summarizes the cell and molecular biology of the OXTR and its downstream signaling cascades, particularly focusing on the vasoactive functions of OXTR signaling in humans and animal models, as well as the clinical applications of OXTR targeting cerebrovascular accidents.

show abstract

Section: Oxidative and Inflammatory Stressmentioning

confidence: 91%

Section: Cellular Differentiationmentioning

confidence: 99%

Oxytocin Receptor Signaling in Vascular Function and Stroke

McKay

Counts

2020

Front. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Involvement SAFE pathway in cardioprotection. Kobayashi et al, 2009;Anvari et al, 2012;Polshekan et al, 2016Polshekan et al, , 2019 OT treatment in simulated ischemia reperfusion.…”

Section: Oxytocin and Inflammationmentioning

confidence: 99%

“…Activation of protein kinase C (PKC) by DAG signals pro-survival ERK and downstream targets, and intracellular Ca 2+ mobilization stimulates the release of ANP from CMC (Schiebinger, 1989). Cardioprotection via phosphoinositide-3-kinases (PI3K)/Akt and NO has been reported with OT (Kobayashi et al, 2009;Florian et al, 2010;Polshekan et al, 2016). Moreover, in a rabbit model of MI, activation of STAT3 and ERK, key molecules that mediate FIGURE 3 | Schematic diagram of hypothetical OT signaling pathways targeting the nucleus and mitochondria in the cardiac cells.…”

Section: Molecular Signaling Of Oxytocin In the Heartmentioning

confidence: 99%

“…Stimulation of these pathways with OT reduces the force and rate of contraction (Mukaddam-Daher et al, 2001), promotes vasodilation (Jankowski et al, 2000), and provides protection against MI in rats preconditioned with OT (Jankowski et al, 2010b;Ondrejcakova et al, 2012). However, Polshekan et al (2016) have demonstrated by using the isolated perfused rat heart model that OT exhibits anti-ischemic effects when acutely administered at the onset of reperfusion. Similarly, we also demonstrated this protective effect using H9c2 cells exposed to experimental IR in the presence of OT with optical effects of OT observed at the onset of reperfusion (Gonzalez-Reyes et al, 2015).…”

Section: Oxytocin In Pathways Of Cardioprotectionmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Oxytocin in Cardiovascular Protection

2020

View full text Add to dashboard Cite

Our research in the last two decades on oxytocin (OT) in heart biology has generated a broad interest of the role of this neuropeptide on overall cardiometabolic and vascular functions. Our important findings highlighted the discovery of a specific OT system, including the presence of OT and the OT receptor (OTR) in the rodent and human heart (Gutkowska et al., 1997; Jankowski et al., 1998). The presence of OT and OTRs in cardiac chambers indicates autocrine and/or paracrine roles for this peptide. The effects of OT and its associated signaling pathways are mediated by OTRs, which are also present in large vessels (Jankowski et al., 1998, 2000) as well as in cardiac microvessels expressing the CD31 marker and co-localizing with endothelial nitric oxide (NO)

show abstract

Cardioprotection by post-conditioning with exogenous triiodothyronine in isolated perfused rat hearts and isolated adult rat cardiomyocytes

et al. 2021

View full text Add to dashboard Cite

Ischemic post-conditioning (iPoCo) by coronary re-occlusion/reperfusion during immediate reperfusion after prolonged myocardial ischemia reduces infarct size. Mechanical manipulation of culprit lesions, however, carries the risk of coronary microembolization which may obscure iPoCo’s cardioprotection. Pharmacological post-conditioning with exogenous triiodothyronine (T3) could serve as an alternative conditioning strategy. Similar to iPoCo, T3 may activate cardioprotective prosurvival pathways. We aimed to study T3’s impact on infarct size and its underlying signal transduction. Hearts were isolated from male Lewis rats (200–380 g), buffer-perfused and subjected to 30 min/120 min global zero-flow ischemia/reperfusion (I/R). In additional hearts, either iPoCo (2 × 30 s/30 s I/R) was performed or T3 (100–500 µg/L) infused at reperfusion. Infarct size was demarcated with triphenyl tetrazolium chloride staining and calculated as percent of ventricular mass. Infarct size was reduced with iPoCo to 16 ± 7% vs. 36 ± 4% with I/R only. The maximum infarct size reduction was observed with 300 µg/L T3 (14 ± 2%). T3 increased the phosphorylation of protein kinase B and mitogen extracellular-regulated-kinase 1/2, both key enzymes of the reperfusion injury salvage kinase (RISK) pathway. Pharmacological RISK blockade (RISK-BL) during reperfusion abrogated T3’s cardioprotection (35 ± 10%). Adult ventricular cardiomyocytes were isolated from buffer-perfused rat hearts and exposed to 30 min/5 min hypoxia/reoxygenation (H/R); reoxygenation was initiated without or with T3, respectively, and without or with RISK-BL, respectively. Maximal preservation of viability was observed with 500 µg/L T3 after H/R (27 ± 4% of all cells vs. 5 ± 3% in time-matched controls). Again, RISK-BL abrogated protection (11 ± 3%). Mitochondria were isolated at early reperfusion from buffer-perfused rat hearts without or with iPoCo or 300 µg/L T3, respectively, at reperfusion. T3 improved mitochondrial function (i.e.: increased respiration, adenosine triphosphate production, calcium retention capacity, and decreased reactive oxygen species formation) to a similar extent as iPoCo. T3 at reperfusion reduces infarct size by activation of the RISK pathway. T3’s protection is a cardiomyocyte phenomenon and targets mitochondria.

show abstract

RISK pathway is involved in oxytocin postconditioning in isolated rat heart

Cited by 16 publications

References 58 publications

Oxytocin Receptor Signaling in Vascular Function and Stroke

Oxytocin Receptor Signaling in Vascular Function and Stroke

The Role of Oxytocin in Cardiovascular Protection

Cardioprotection by post-conditioning with exogenous triiodothyronine in isolated perfused rat hearts and isolated adult rat cardiomyocytes

Contact Info

Product

Resources

About