Heat shock protein 22 reduces phenylephrine-induced cardiomyocytes hypertrophy
10.3760/cma.j.issn.1671-0282.2019.03.013
- VernacularTitle:热休克蛋白22减轻苯肾上腺素诱导的心肌细胞肥大反应
- Author:
Lili XIAO
1
;
Yulei GU
;
Lu GAO
;
Jun CHEN
;
Xiaofang WANG
;
Ling LI
Author Information
1. 郑州大学第一附属医院心血管内科 450052
- Keywords:
Heat shock protein 22;
Phenylephrine;
Cardiomyocytes hypertrophy;
Oxidative stress;
AMP-activated protein kinase α
- From:
Chinese Journal of Emergency Medicine
2019;28(3):344-349
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of Hsp22 on phenylephrine-induced cardiomyocytes hypertrophy.Methods Primary rat myocardial cells were isolated and cultured in Department of Cardiology,the First Affiliated Hospital of Zhengzhou University.Cells were divided into four groups randomly:Control group,model group,treatment group with 1 μg/mL Hsp22,and treatment group with 10 μg/mL Hsp22.Phenylephrine stimuli was used to induce cardiomyocytes hypertrophy model.Cell viability was measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.Cardiomyocytes surface area was evaluated by α-actin immunofluorescence staining.Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the transcription level of hypertrophic markers.Reactive oxygen species level was detected by 2',7'-Dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe.Apoptosis was detected by TUNEL staining.Signal pathway protein expression was detected by Western blot.SPSS 13.0 was used for statistical analysis.Data were expressed as mean + standard deviation.All data were analyzed by one-way ANOVA between groups.Comparisons between two groups were performed using LSD-t test.A P＜0.05 was considered statistically significant.Results Different concentrations of Hsp22 had no effect on cardiomyocytes viability (F=6.622;P＞0.05).Phenylephrine stimulation significantly increased cardiomyocytes area (t=10.80;P＜0.05),increased the transcription level of hypertrophy markers atrial natriuretic peptide (t=37.72;P＜0.05),type B natriuretic peptide (t=16.85;P＜0.05),and myosin heavy chain beta (t=41.53;P＜0.05).Different concentrations of Hsp22 significantly reduced cardiomyocytes area (PE+ 1 μg/mL Hsp22 t=4.018;P＜0.05;PE+10 μg/mL Hsp22 t=10.80;P＜0.05),reduced the transcription level of hypertrophic markers atrial natriuretic peptide (PE+1 μg/mL Hsp22 t=27.12,P＜0.05;PE+10 μg/mL Hsp22 t=37.72,P＜0.05),type B natriuretic peptide (PE+1 μg/mL Hsp22 t=4.82,P＜0.05;PE+10 μg/mL Hsp22 t=12.74,P＜0.05),and myosin heavy chain beta (PE+1 μg/mL Hsp22 t=23.68,P＜0.05;PE+10 μg/mL Hsp22 t=30.54,P＜0.05).Westem blot showed that Hsp22 increased the activation of AMP-activated protein kinase α (PE+1 μg/mL Hsp22 t=5.89,P＜0.05;PE+10 μg/mL Hsp22 t=5.88,P＜0.05),reduced mTOR phosphorylation level (PE+1 μg/mL Hsp22 t=16.80,P＜0.05;PE+10.μg/mL Hsp22 t=20.46,P＜0.05).Conclusions Hsp22 inhibits cardiomyocytes hypertrophy by activating AMP-activated protein kinase α.Hsp22 may become a potential anti-hypertrophic drug.
