The protective effect of microRNA-320 on left ventricular remodeling after myocardial ischemia-reperfusion injury in the rat model.
The protective effect of microRNA-320 on left ventricular remodeling after myocardial ischemia-reperfusion injury in the rat model.
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DOI：
10.3390/ijms151017442
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发表时间：
2014-09-29
影响因子：
5.6
通讯作者：
Li Q
中科院分区：
文献类型：
--
作者：
Song CL;Liu B;Diao HY;Shi YF;Li YX;Zhang JC;Lu Y;Wang G;Liu J;Yu YP;Guo ZY;Wang JP;Zhao Z;Liu JG;Liu YH;Liu ZX;Cai D;Li Q
本研究的主要目的是研究microRNA-320 （miR-320）在心肌缺血再灌注（I/R）损伤大鼠模型左心室重构中的作用，探讨miR-320介导的心肌保护的心肌机制。本研究取雄性Wistar大鼠120只（240 ~ 280 g），随机分为3组：(1)假手术组（假手术组：n = 40）；(2)缺血再灌注模型组（I/R组：n = 40）；(3)安他哥米尔-320组I/R模型（I/R +安他哥米尔-320组n = 40）。记录各组术后各时间点（第1天、第3天、第7天、第15天、第30天）经食管超声心动图心功能值变化。心肌切片采用苏木精和伊红染色（H&E），光学显微镜下观察。采用天狼星红染色评价心肌纤维化程度。采用末端dUTP缺口末端标记法（TUNEL）和qRT-PCR法检测细胞凋亡率，测定心肌组织中miR-320的表达水平。经食管超声心动图显示，I/R组左室射血分数（LVEF）、左室分数缩短（LVFS）、左室收缩压（LVSP）及±dp/dtmax值明显低于假手术组，左室舒张末期压（LVEDP）值高于假手术组。I/R组LVEF、LVFS、LVSP及±dp/dtmax值随再灌注时间延长呈逐渐降低趋势，LVEDP值呈上升趋势。H&E染色显示，I/R组大鼠心肌组织出现广泛的心肌损伤；I/R + antagomir-320组心肌细胞损伤程度明显优于I/R组。天狼星红染色结果显示，随着再灌注时间的延长，I/R组心肌纤维化程度加重。I/R + antagomir-320组心肌纤维化程度较I/R组轻。与I/R组相比，sham组和I/R + antagomir-320组的细胞凋亡率均较低。qRT-PCR结果显示，miR-320在I/R组中的表达明显高于sham组和I/R + antagomir-320组。miR-320在心肌I/R损伤大鼠模型中表达水平显著上调，可能与心肌I/R损伤引发的左室重构的预防有关。
The primary objective of this study investigated the role of microRNA-320 (miR-320) on left ventricular remodeling in the rat model of myocardial ischemia-reperfusion (I/R) injury, and we intended to explore the myocardial mechanism of miR-320-mediated myocardium protection. We collected 120 male Wistar rats (240–280 g) in this study and then randomly divided them into three groups: (1) sham surgery group (sham group: n = 40); (2) ischemia-reperfusion model group (I/R group: n = 40); and (3) I/R model with antagomir-320 group (I/R + antagomir-320 group: n = 40). Value changes of heart function in transesophageal echocardiography were recorded at various time points (day 1, day 3, day 7, day 15 and day 30) after surgery in each group. Myocardial sections were stained with hematoxylin and eosin (H&E) and examined with optical microscope. The degree of myocardial fibrosis was assessed by Sirius Red staining. Terminal dUTP nick end-labeling (TUNEL) and qRT-PCR methods were used to measure the apoptosis rate and to determine the miR-320 expression levels in myocardial tissues. Transesophageal echocardiography showed that the values of left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP) and ±dp/dtmax in the I/R group were obviously lower than those in the sham group, while the left ventricular end-diastolic pressure (LVEDP) value was higher than that in the sham group. The values of LVEF, LVFS, LVSP and ±dp/dtmax showed a gradual decrease in the I/R group, while the LVEDP value showed an up tendency along with the extension of reperfusion time. The H&E staining revealed that rat myocardial tissue in the I/R group presented extensive myocardial damage; for the I/R + antagomir-320 group, however, the degree of damage in myocardial cells was obviously better than that of the I/R group. The Sirius Red staining results showed that the degree of myocardial fibrosis in the I/R group was more severe along with the extension of the time of reperfusion. For the I/R + antagomir-320 group, the degree of myocardial fibrosis was less severe than that in the I/R group. Tissues samples in both the sham and I/R + antagomir-320 groups showed a lower apoptosis rate compared to I/R group. The qRT-PCR results indicated that miR-320 expression in the I/R group was significantly higher than that in both the sham and I/R + antagomir-320 groups. The expression level of miR-320 is significantly up-regulated in the rat model of myocardial I/R injury, and it may be implicated in the prevention of myocardial I/R injury-triggered left ventricular remodeling.
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影响因子：
3.7
作者：
Miyazaki Y;Ikeda Y;Shiraishi K;Fujimoto SN;Aoyama H;Yoshimura K;Inui M;Hoshijima M;Kasahara H;Aoki H;Matsuzaki M
通讯作者：
Matsuzaki M
影响因子：
2.1
作者：
Gidlöf O;Smith JG;Miyazu K;Gilje P;Spencer A;Blomquist S;Erlinge D
通讯作者：
Erlinge D
G 蛋白偶联受体激酶 2 (GRK2) 的心肌消融通过抗内在凋亡途径减少缺血/再灌注损伤。
影响因子：
3.7
作者：
Fan Q;Chen M;Zuo L;Shang X;Huang MZ;Ciccarelli M;Raake P;Brinks H;Chuprun KJ;Dorn GW 2nd;Koch WJ;Gao E
通讯作者：
Gao E
影响因子：
37.8
作者：
Burchfield JS;Xie M;Hill JA
通讯作者：
Hill JA
DOI：
10.2215/cjn.00430111
发表时间：
2011-07-01
影响因子：
9.8
作者：
Lorenzen, Johan M.;Kielstein, Jan T.;Thum, Thomas
通讯作者：
Thum, Thomas