Glucose Fluctuations Aggravate Cardiac Susceptibility to Ischemia/Reperfusion Injury by Modulating MicroRNAs Expression

Saito, Shotaro; Thuc, Luong Cong; Teshima, Yasushi; Nakada, Chisato; Nishio, S.; Kondo, Hidekazu; Fukui, Atsushi; Abe, Ichitaro; Ebata, Yuki; Saikawa, Tetsunori; Moriyama, Masatsugu; Takahashi, Naohiko

doi:10.1253/circj.cj-14-1218

Cited by 34 publications

(40 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…20 found 3.67 fold of control group in heart failure patients [39] and after glucose fluctuations [40], it is similar in our study (3.386 fold of control), it suggests that let-7e might be an active role in the pathogenesis of heart failure, so the aberrant expression of let-7e might result in congenital heart disease.…”

Section: Accepted Manuscriptsupporting

confidence: 86%

Specific MicroRNAs comparisons in hypoxia and morphine preconditioning against hypoxia-reoxgenation injury with and without heart failure

Zhu¹,

Han

et al. 2017

Life Sciences

View full text Add to dashboard Cite

Section: Accepted Manuscriptsupporting

confidence: 86%

Specific MicroRNAs comparisons in hypoxia and morphine preconditioning against hypoxia-reoxgenation injury with and without heart failure

Zhu¹,

Han

et al. 2017

Life Sciences

View full text Add to dashboard Cite

“…18 Moreover, miR-200c is abundantly expressed in the heart and, in the diabetic heart, is involved in myocardial injury induced by glucose fluctuations that, result in an increase in the levels of ROS. 19 On the basis of these findings, we suggested a pos- 20,21 In brief, all animals were anaesthetized with chloral hydrate (300 mg/kg, ip). Aortic banding was created around the abdominal aorta using a 7-0 silk suture and a 22-gauge needle.…”

Section: Introductionmentioning

confidence: 99%

Down‐regulation of miR‐200c attenuates AngII‐induced cardiac hypertrophy via targeting the MLCK‐mediated pathway

Huang

Cheng

Guo

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

Background MicroRNAs (miRNAs) have been shown to commonly contribute to cardiac hypertrophy (CH). The aim of this study was to test the hypothesis that miR‐200c plays an important role in the progression of CH by targeting myosin light chain kinase (MLCK/MYLK). Methods and results Cardiac hypertrophy was induced by aortic banding (AB) in rats. Cellular hypertrophy in neonatal rat cardiomyocytes (NCMs) was induced by AngII treatment. Echocardiography, histology and molecular measurements were used to assess the results of the experiments. The levels of apoptosis and reactive oxygen species (ROS) were also measured. Quantitative real‐time PCR (qRT‐PCR) and Western blotting were used to measure mRNA and protein levels respectively. The present results showed that miR‐200c expression was increased in response to CH both in vivo and in vitro. The down‐regulation of miRNA‐200c by a specific inhibitor markedly ameliorated CH resulting from AngII treatment, and the mRNA levels of atrial natriuretic peptide, brain natriuretic peptide and β‐myosin heavy chain were simultaneously decreased. Notably, minimal apoptosis and ROS accumulation were identified in AngII‐induced hypertrophic cardiomyocytes. Conversely, the up‐regulation of miR‐200c using specific mimics reversed these effects. Mechanistic investigations demonstrated that the MLCK gene is a direct target of miR‐200c; an increase in miR‐200c levels led to a decrease in the expression of MLCK and its downstream effector, p‐MLC2, while miR‐200c inhibition increased the expression of these proteins. Furthermore, inhibiting MLCK impaired the anti‐hypertrophic effects contributions produced by the knockdown of miR‐200c. Conclusion Our studies suggest that miR‐200c may serve as a potential therapeutic target that could delay hypertrophy. We have also uncovered a relationship between miR‐200c and MLCK, identifying MLCK as a direct mediator of miR‐200c.

show abstract

“…Cardiac ventricular myocytes were obtained from 1‐ to 3‐day‐old Sprague Dawley rats and cultured as described elsewhere . Briefly, cardiac ventricles were removed and digested with trypsin (2 mg/mL) at 37°C.…”

Section: Methodsmentioning

confidence: 99%

“…Cardiac ventricular myocytes were obtained from 1-to 3-dayold Sprague Dawley rats and cultured as described elsewhere. 11 Briefly, cardiac ventricles were removed and digested with trypsin (2 mg/mL) at 37°C. Cardiomyocytes were then isolated and cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 5% foetal bovine serum, penicillin (100 U/ mL), streptomycin (100 mg/mL) and vitamin B 12 (2 µg/mL).…”

Section: Primary Culture Of Neonatal Rat Cardiomyocytesmentioning

confidence: 99%

Hyponatraemia aggravates cardiac susceptibility to ischaemia/reperfusion injury

Oniki

Teshima

Nishio

et al. 2019

Int J Experimental Path

Self Cite

View full text Add to dashboard Cite

Summary Hyponatraemia is defined as a serum sodium concentration of <135 mEql/L and is the most common electrolyte disturbance in patients with chronic heart failure. We hypothesize that hyponatraemia may induce Ca2+ overload and enhance reactive oxygen species (ROS) production, which will exacerbate myocardial injury more than normonatraemia. We investigated the effect of hyponatraemia on the ability of the heart to recover from ischaemia/reperfusion episodes. Cardiomyocytes were obtained from 1‐ to 3‐day‐old Sprague Dawley rats. After isolation, cardiomyocytes were placed in Dulbecco's modified Eagle's medium (DMEM) containing low sodium concentration (110, 120, or 130 mEq/L) or normal sodium concentration (140 mEq/L) for 72 hours. Exposure of cardiomyocytes to each of the low‐sodium medium significantly increased both ROS and intracellular Ca2+ levels compared with the exposure to the normal‐sodium medium. In vivo, 8‐week‐old male Sprague Dawley rats were divided into four groups: control group (Con), furosemide group (Fur), low‐sodium diet group (Lsd) and both furosemide and low‐sodium diet group (Fur + Lsd). The hearts subjected to global ischaemia exhibited considerable decrease in left ventricular developed pressure during reperfusion, and the size of infarcts induced by ischaemia/reperfusion significantly increased in the Fur, Lsd and Fur + Lsd compared with that in the Con. Hyponatraemia aggravates cardiac susceptibility to ischaemia/reperfusion injury by Ca2+ overload and increasing in ROS levels.

show abstract

Glucose Fluctuations Aggravate Cardiac Susceptibility to Ischemia/Reperfusion Injury by Modulating MicroRNAs Expression

Cited by 34 publications

References 32 publications

Specific MicroRNAs comparisons in hypoxia and morphine preconditioning against hypoxia-reoxgenation injury with and without heart failure

Specific MicroRNAs comparisons in hypoxia and morphine preconditioning against hypoxia-reoxgenation injury with and without heart failure

Down‐regulation of miR‐200c attenuates AngII‐induced cardiac hypertrophy via targeting the MLCK‐mediated pathway

Hyponatraemia aggravates cardiac susceptibility to ischaemia/reperfusion injury

Contact Info

Product

Resources

About