Role of reverse mode Na+/Ca2+ exchanger in the cardioprotection of metabolic inhibition preconditioning in rat ventricular myocytes

Li, Shuzhuang; Wu, Feng; Wang, Bo; Wei, Geng-Ze; Jin, Zhenxiao; Zang, Yi-Min; Zhou, Jing‐Jun; Wong, Tak‐Ming

doi:10.1016/j.ejphar.2006.12.036

Cited by 15 publications

(10 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies about the protective effect of melatonin on IR injury in various organs showed that melatonin can eliminate free radicals, inhibit release of inflammatory media and apoptosis [8][9][10] . On the other hand, many factors can result in IR injury, such as free radicals [11] , overload of calcium [12] , inflammation of white blood cells and vascular endothelial cells [13] and apoptosis, etc [14] . Therefore, we detected serum TNF-α, MDA and ICAM-1-stained cells in liver tissues in this study.…”

Section: Applicationsmentioning

confidence: 99%

Melatonin protects liver from intestine ischemia reperfusion injury in rats

Li¹,

Yin²,

Gu³

et al. 2008

WJG

View full text Add to dashboard Cite

AIM:To investigate the protective effect of melatonin on liver after intestinal ischemia-reperfusion injury in rats. METHODS: One hundred and fifty male Wistar rats, weighing 190-210 g, aged 7 wk, were randomly divided into melatonin exposure group, alcohol solvent control group and normal saline control group. Rats in the melatonin exposure group received intraperitoneal (IP) melatonin (20 mg/kg) 30 min before intestinal ischemia-reperfusion (IR), rats in the alcohol solvent control group received the same concentration and volume of alcohol, and rats in the normal saline control group received the same volume of normal saline. Serum samples were collected from each group 0.5, 1, 6, 12, and 24 h after intestinal IR. Levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured with an auto-biochemical analyzer. Serum TNF-α was tested by enzyme-linked immunosorbent assay (ELISA). Malondialdehyde (MDA) in liver was detected by colorimetric assay. Pathological changes in liver and immunohistochemical straining of ICAM-1 were observed under an optical microscope. RESULTS: The levels of ALT measured at various time points after intestinal IR in the melatonin exposure group were significantly lower than those in the other two control groups (P < 0.05). The serum AST levels 12 and 24 h after intestinal IR and the ICAM-1 levels (%) 6, 12 and 24 h after intestinal IR in the melatonin exposure group were also significantly lower than those in the other two control groups (P < 0.05). CONCLUSION: Exotic melatonin can inhibit the activity of ALT, AST and TNF-α, decrease the accumulation of MDA, and depress the expression of ICAM-1 in liver after intestinal IR injury, thus improving the liver function.

show abstract

Section: Applicationsmentioning

confidence: 99%

Melatonin protects liver from intestine ischemia reperfusion injury in rats

Li¹,

Yin²,

Gu³

et al. 2008

WJG

View full text Add to dashboard Cite

show abstract

“…Very recently, Sisalli et al [36] demonstrated that NCX1 has a key role in preconditioning-induced neuroprotection owing to its ability to control calcium homeostasis in the endoplasmic reticulum (ER). In accordance with the role of NCX1 as a mediator of tolerance in the brain, it has been demonstrated that this exchanger isoform also seems to elicit the cardioprotective effects of ischemic or H 2 S-induced preconditioning in cardiomyocytes [37,15].…”

Section: Discussionmentioning

confidence: 91%

NCX1 Exchanger Cooperates with Calretinin to Confer Preconditioning-Induced Tolerance Against Cerebral Ischemia in the Striatum

et al. 2015

View full text Add to dashboard Cite

Recently, the Na(+)/Ca(+2) exchanger NCX1 and the calcium binding protein calretinin have emerged as new molecular effectors of delayed preconditioning in the brain. In the present study, we investigated whether NCX1 and calretinin cooperate within the preconditioned striatum to confer neurons greater resistance to degeneration. Confocal microscopy analysis revealed that NCX1 expression was upregulated in calretinin-positive interneurons in the rat striatum after tolerance induction. Consistently, coimmunoprecipitation assays performed on human SHSY-5Y cells, a neuronal cell line which constitutively expresses calretinin, revealed a binding between NCX1 and calretinin. Finally, silencing of calretinin expression, both in vitro and in vivo, significantly prevented preconditioning-induced neuroprotection. Interestingly, our biochemical and functional studies showed that the selective silencing of calretinin in brain cells significantly prevented not only the preconditioning-induced upregulation of NCX1 expression and activity but also the activation of the prosurvival protein kinase Akt, which is involved in calretinin and NCX1 protective actions. Collectively, our results indicate that the Na(+)/Ca(+2) exchanger NCX1 and the calcium binding protein calretinin cooperate within the striatum to confer tolerance against cerebral ischemia.

show abstract

“…[Ca 2+ ] i was measured by the fluorescent calcium indicator Fura-2 in a dual-fluorescence, calcium ion-sensing system (IonOptix, Milton, MA) [16]. Cells were loaded with Fura-2/AM as described previously [16,17].…”

Section: Measurement Of Resting Intracellular Ca 2+ ([Ca 2+ ] I ) Andmentioning

confidence: 99%

“…After that, cells were exposed to Na + -free Tyrode solution for 3 min together with ryanodine and thapsigargin, and then reperfused with normal Tyrode solution to determine the reverse-mode NCX activity [16,20]. The Na + -free Tyrode solution was prepared by substituting Na + with 125 mM Nmethyl-D-glucamine (NMDG) [16].…”

Section: Measurement Of Reverse-mode Ncx Activitymentioning

confidence: 99%

“…Ventricular myocytes were isolated from male SpragueDawley rats (200-250 g), by a collagenase perfusion method routinely used in our lab as described previously [16]. Briefly, the hearts were rapidly removed after decapitation and retrogradely perfused for 5 min at 37°C with oxygenated normal Tyrode solution contained (in mM) 140 NaCl, 4.2 KCl, 1.2 MgCl 2 , 1.25 CaCl 2 , 1.2 KH 2 PO 4 , 10 glucose, and 10 HEPES (adjusted to pH 7.4 with NaOH), followed by 5 min with Ca 2+ -free Tyrode solution.…”

Section: Isolation Of Ventricular Myocytesmentioning

confidence: 99%

See 1 more Smart Citation

Low extracellular K+ increases intracellular Ca2+ oscillation and injury by activating the reverse mode Na+–Ca2+ exchanger and inhibiting the Na+, K+ ATPase in rat cardiomyocytes

Role of reverse mode Na+/Ca2+ exchanger in the cardioprotection of metabolic inhibition preconditioning in rat ventricular myocytes

Cited by 15 publications

References 34 publications

Melatonin protects liver from intestine ischemia reperfusion injury in rats

Melatonin protects liver from intestine ischemia reperfusion injury in rats

NCX1 Exchanger Cooperates with Calretinin to Confer Preconditioning-Induced Tolerance Against Cerebral Ischemia in the Striatum

Low extracellular K+ increases intracellular Ca2+ oscillation and injury by activating the reverse mode Na+–Ca2+ exchanger and inhibiting the Na+, K+ ATPase in rat cardiomyocytes

Contact Info

Product

Resources

About