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[1]侯维纳,吕爱婷,孙琪青,等.MIR-138-5p 通过靶向组蛋白去乙酰化酶调节心脏 肥大[J].天津医科大学学报,2022,28(03):248-252.
　HOU Wei-na,LYU Ai-ting,SUN Qi-qing,et al.MIR-138-5p regulates cardiac hypertrophy by targeting histone deacetylase[J].Journal of Tianjin Medical University,2022,28(03):248-252.
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MIR-138-5p 通过靶向组蛋白去乙酰化酶调节心脏 肥大(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
28卷
期数:
2022年03期
页码:
248-252
栏目:
心血管疾病专题
出版日期:
2022-05-20

文章信息/Info

Title:
MIR-138-5p regulates cardiac hypertrophy by targeting histone deacetylase
文章编号:
1006-8147(2022)03-0248-05
作者:
侯维纳; 吕爱婷; 孙琪青; 冯迎军
（郑州大学附属儿童医院，河南省儿童医院，郑州儿童医院心内科，郑州450000）
Author(s):
HOU Wei-na; LYU Ai-ting; SUN Qi-qing; FENG Ying-jun
（Department of Cardiology，Children′s Hospital Affiliated to Zhengzhou University，Henan Children′s Hospital，Zhengzhou Children′s Hospital，East Third Street，Zhengzhou 450000，China）
关键词:
MIR-138-5p; 靶向; 组蛋白去乙酰化酶; 心脏肥大
Keywords:
miR-138-5p; targeting; histonedeacetylase; cardiachypertrophy
分类号:
R541
DOI:
-
文献标志码:
A
摘要:
目的：探究MIR-138-5p 对心脏肥大的影响及其机制。方法：首先构建体外心脏肥大的模型，HE 染色、α-肌动蛋白染色 和RT-PCR 方法，分别检测模型大鼠心脏的横断面积和血管紧张素Ⅱ（AngⅡ）处理的心肌细胞（H9c2）的表面积和心肌细胞中 MIR-138-5p mRNA 表达情况；MIR-138-5p-mimic 转染AngⅡ处理过的H9c2 细胞，α-肌动蛋白染色和Western 印迹分别检测 心肌细胞的表面积和心肌肥大标志物的蛋白表达水平；采用TargetScan 在线软件筛选miR-138-5p 的潜在靶基因，并进一步验 证。MIR-138-5p-mimic、pcDNA- HDAC4共转染AngⅡ处理过的H9c2 细胞，α-肌动蛋白染色和Western 印迹法分别检测心肌 细胞的表面积和心肌肥大标志物的蛋白表达水平。结果：相对于Sham 组，模型大鼠的心脏体积及心脏横截面均明显增大，心肌 细胞中的MIR-138-5p mRNA 表达水平明显降低（F=21.578，P<0.001）；相对于Con 组，AngⅡ组心肌细胞的表面积明显增大，且 MIR-138-5p mRNA 表达水平明显降低（F=23.790，P<0.001）。相对于AngⅡ+miR-NC 组，AngⅡ+miR-mimic 组心肌细胞的表面 积（F=8.325，P<0.01）、心肌肥大标志蛋白表达水平（F=9.532，P<0.01）和心肌细胞中HDAC4 mRNA表达水平明显降低（F=25.530， P<0.001）； 相对于MIR-138-5p-mimic+pcDNA-Con 组，MIR-138-5p- mimic+pcDNA-HDAC4 组心肌细胞的表面积明显减小 （F=10.134，P<0.01），心肌肥大标志蛋白表达水平明显升高。结论：MIR-138-5p 通过靶向组蛋白脱乙酰基酶-8（HDAC4） 调节心脏肥大反应。
Abstract:
Objective：To explore the effect of MIR-138-5p on cardiac hypertrophy and its mechanism. Methods: Firstly，the model of cardiac hypertrophy in vitro was constructed. HE staining，α-actin staining and RT-PCR were used to detect the cross-sectional area of the model rat heart，the surface area of AngⅡ-treated cardiomyocytes（H9c2）and the expression ofMIR-138-5pmRNA in the cardiomyocytes. MIR-138-5p-mimic was transfected into H9c2 cells treated with AngⅡ，α-actin staining and Western-blotting were used to detect the surface area of cardiomyocytes and the protein expression level of cardiachypertrophy markers. TargetScan online software was used to screen potential target genes of MIR-138-5p and further verify. MIR-138-5p-mimic，pcDNA-histone deacetylase-4（HDAC4）were co -transfected into H9c2 cells treated with AngⅡ，α -actin staining and Western -blotting was used to detect the surface area of cardiomyocytes and the protein expression level of cardiac hypertrophy markers. Results: Compared with the Sham group，the heart volume and heart cross -section of model rats were significantly increased，and the expression level of MIR -138 -5p mRNA in cardiomyocytes was significantly decreased（F=21.578，P <0.001）. Compared with the Con group，the surface area of cardiomyocytes in the AngⅡgroup was significantly increased，and the expression level of MIR-138-5p mRNA was significantly reduced（F=23.790，P <0.001）. Compared with the AngⅡ+ miR-NC group，the surface area of cardiomyocytes （F=8.325，P<0.01）and the expression of cardiac hypertrophy marker proteins in the AngⅡ+ miR-mimic group were significantly reduced（F=9.532，P <0.01）. Compared with the AngⅡ +miR-NC group，the AngⅡ+miR-mimic group was found the expression level of HDAC4 mRNA in cardiomyocytes was significantly reduced（F=25.530，P<0.001）. Compared with the MIR-138-5p-mimic+pcDNA-Con group，the surface area of cardiomyocytes in the MIR-138-5p-mimic+pcDNA-HDAC4 group was significantly reduced（F=10.134，P <0.01），and the expression level of cardiac hypertrophy marker protein was obviously elevated. Conclusion：MIR-138-5p regulates cardiac hypertrophy by targeting HDAC4.

参考文献/References:

[1] SHIMIZU I，MINAMINO T. Physiological and pathologicalcardiac hypertrophy[J]. J Mol Cell Cardiol，2016，97：245-262.
[2] THAM Y K，BERNARDO B C，OOI J Y，et al.Pathophysiology of cardiac hypertrophy and heartfailure：signaling pathways and novel therapeutic targets[J]. ArchToxicol，2015，89（9）：1401-1438.
[3] XIAO Y，XU J Y，YIN W K.Aberrant epigenetic modifications of noncoding RNAs in human disease[J]. Adv Exp Med Biol，2018，1094： 65-75.
[4] 唐夏莉，焦德敏，陈君，等. miRNA-126 对肺癌A549 细胞的增 殖、迁移、侵袭及EGFR/AKT/mTOR 信号通路的影响[J].中国病 理生理杂志，2016，32（3）：458-463.
[5] CHEN Z Y，CHEN F，CAO N，et al. miR-142-3p contributes to early cardiac fate decision of embryonic stem cells[J]. Stem Cells Int， 2017，6（5）：1-10.
[6] ROBERTO G M，LIRA R C，DELSIN L E，et al. microRNA-138-5p as a worseprognosis biomarker in pediatric，adolescent，and young adult osteosarcoma[J]. Pathol Oncol Res，2020，26（2）：877-883.
[7] LIU L，WANG C，SUN D，et al.Calhex ameliorates cardiac hypertrophy by inhibiting cellular autophagy in vivo and in vitro [J].Cell Physiol Biochem，2015，36（4）：1597-1612.
[8] FREY N，OLSON E N. Cardiac hypertrophy：the good，thebad，and the ugly[J]. Annu Rev Physiol，2003，65：45-79.
[9] LIU B L，CHENG M，HU S，et al.Overexpression of miR-142 -3p improves mitochondrial function in cardiac hypertrophy [J].Biomed Pharmacother，2018，（108）：1347-1356.
[10] XUWF，CHEN B，KE D，et al.MicroRNA-138-5p targets the NFIBSnail1axis to inhibit colorectal cancer cell migrationand chemoresistance[ J].Cancer Cell Int，2020，20：475.
[11] YANG R，LIU M，LIANG H，et al. miR-138-5p contributes to cell proliferation andinvasion by targeting survivin in bladder cancer cells[J]. Mol Cancer，2016，15（1）：82.
[12] AMODIO N，STAMATO M A，GULL魨A M，et al. Therapeutic targeting of miR-29b/HDAC4 epigenetic loop in multiple myeloma[J]. Mol Cancer Ther，2016，15（6）：1364-1375.
[13] YANG D，XIAO CX，LONG F，et al.HDAC4 regulates vascular inflammation via activation of autophagy [J].Cardiovasc Res，2018， 114（7）：1016-1028.
[14] BROIDE R S，REDWINE J M，AFTAHI N，et al. Distribution of histone deacetylases 1-11 in the rat brain[J]. J Mol Neurosci，2007， 31（1）：47-58.
[15] PIGNA E，SIMONAZZI E，SANNA K，et al. Histone deacetylase 4 protects from denervation and skeletal muscle atrophy in a murine model of amyotrophic lateral sclerosis[J]. Ebiol Medi，2019，40，717-732.

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备注/Memo

备注/Memo:
基金项目河南省医学科技攻关计划（2018020617）
作者简介:侯维纳（1988-），女，主治医师，硕士，研究方向：小儿心血管；E-mail：houwn1988@163.com。
更新日期/Last Update: 2022-06-01