MiR-30c-2-3p对足细胞活力及Nephrin和Podocin蛋白表达的影响

Abstract
Figure/Table
References (20)
Related Citation (0)

Download: PDF (795 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective To investigate the effect of MiR-30c-2-3p on podocyte viability and Nephrin and Podocin protein expression. Methods The model of mice podocyte injury was induced by puromycin aminonucleoside (PAN) in vitro, the podocytes were divided into four groups: blank group, PAN group, negative plasmids+PAN group, positive plasmids+PAN group. The MiR-30c-2-3p mimics were transiently transfected with LipofectamineTM 2000, the cell viability was detected by Cell Counting Kit-8 (CCK-8), the expression of MiR-30c-2-3p was detected by real-time quantitative PCR (qRT-PCR), the expression of Nephrin and Podocin protein was detected by Western blot. Results ①CCK-8 showed that the viability of PAN group was significantly lower than that of the blank group, the differences were statistically significant (P < 0.01). There was no significant difference between the negative plasmid+PAN group and the PAN group (P > 0.05). The viability of positive plasmid+PAN group was significantly increased than that of the PAN group and the negative plasmid+PAN group, the differences were statistically significant (P < 0.05 or P < 0.01). ②The expression of MiR-30c-2-3p in the PAN group was significantly lower than that in the blank group, the differences were statistically significant (P < 0.01). There was no significant difference between the negative plasmid group and the PAN group (P > 0.05). The content of MiR-30c-2-3p in the positive plasmid+PAN group was significantly higher than that of the PAN group and the negative plasmid+PAN group, the differences were statistically significant (P < 0.05 or P < 0.01). ③The expression of Nephrin and Podocin in the PAN group were significantly lower than those in the blank group, the differences were statistically significant (P < 0.01). There was no significant difference between the negative plasmid+PAN group and the PAN group (P > 0.05). Compared with the PAN group and the negative plasmid+PAN group, the expression of Nephrin and Podocin in the positive plasmid+PAN group increased, the differences were statistically significant (P < 0.05). Conclusion The PAN intervention inhibits the podocyte activity, MiR-30c-2-3p content, and the Nephrin and Podocin expression, but the exogenous expression of MiR-30c-2-3p can improve the viability of podocytes and increase the expression of Nephrin and Podocin protein.

Key words： MiR-30c-2-3p Podocyte Puromycin Viability Nephrin Podocin

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors
	CHEN Qi1 MIN Jingjing2 WANG Xiaoyi1▲

Cite this article:

CHEN Qi1 MIN Jingjing2 WANG Xiaoyi1▲. Effects of MiR-30c-2-3p on podocyte viability and expression of Nephrin and Podocin[J]. 中国医药导报, 2017, 14(28): 17-20,30.

URL:

http://www.yiyaodaobao.com.cn/EN/ OR http://www.yiyaodaobao.com.cn/EN/Y2017/V14/I28/17

[1] Wu J，Zheng C，Fan Y，et al. Downregulation of microRNA-30 facilitates podocyte injury and is prevented by glucocorticoids [J]. J Am Soc Nephrol，2013，25（1）：92-104.
[2] 陈楠，任红.原发性局灶节段硬化性肾小球肾炎的治疗进展[J].现代实用医学，2012，24（5）：481-483.
[3] Shi S，Yu L，Chiu C，et al. Podocyte-selective deletion of dicer induces proteinuria and glomerulosclerosis [J]. J Am Soc Nephrol，2008，19（11）：2159.
[4] 朱彩凤，朱斌，李先法，等.原发性局灶节段硬化性肾小球肾炎患者循环microRNA表达谱研究[J].中国中西医结合肾病杂志，2016，17（7）：595-598.
[5] Ambros V. The functions of animal microRNAs [J]. Nature，2004，431（7006）：350-355.
[6] Pandey P，Brors B，Srivastava PK，et al. Microarray-based approach identifies microRNAs and their target functional patterns in polycystic kidney disease [J]. BMC Genomics，2008，9：624.
[7] Kato M，Zhang J，Wang M，et al. MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors [J]. Proc Natl Acad Sci USA，2007，104：3432-3437.
[8] Walsh DW，Roxburgh SA，McGettigan P，et al. Co-regulation of Gremlin and Notch signalling in diabetic nephropathy [J]. Biochim Biophys Acta，2008，1782（1）：10-21.
[9] Dai Y，Sui W，Lan H，et al. Comprehensive analysis of microRNA expression patterns in renal biopsies of lupus nephritis patients [J]. Rheumatol Int，2009，29（7）：749-754.
[10] Dai Y，Sui W，Lan H，et al. Microarray analysis of micro-ribonucleic acid expression in primary immunoglobulin A nephropathy [J]. Saudi Med J，2008，29（10）： 1388-1393.
[11] Tan K，Chen J，Li W，et al. Genome-wide analysis of microRNAs expression profiling in patients with primary IgA nephropathy [J]. Genome，2013，56（3）：161-169.
[12] 朱彩凤，陈琪，朱斌，等.MiR-30c-2-3p对足细胞Nephrin、 Podocin保护作用及雷公藤甲素干预作用研究[J].中国中西医结合肾病杂志，2016，17（7）：952-955.
[13] Chen W，Lin X，Huang J，et al. Integrated profiling of microRNA expression in membranous nephropathy using high-throughput sequencing technology [J]. Int J Mol Med，2014，33（1）：25-34.
[14] Harvey SJ，Jarad G，Cunningham J，et al. Podocyte-specific deletion of dicer alters cytoskeletal dynamics and causes glomerular disease.[J].J Am Soc Nephrol，2008， 19（11）：2150-2158.
[15] Ho J，Ng KH，Rosen S，et al. Podocyte-specific loss of functional microRNAs leads to rapid glomerular and tubular injury [J]. J Am Soc Nephrol，2008，19（11）：2069.
[16] 赵越，张明超，朱小东，等.microRNA-30抑制血管紧张素Ⅱ诱导足细胞损伤的机制[J].肾脏病与透析肾移植杂志，2017，26（1）：14-19.
[17] Wu J，Zheng C，Wang X，et al. MicroRNA-30 family members regulate calcium/calcineurin signaling in podocytes [J]. J Clin Invest，2015，125（11）：4091-4106.
[18] Mitchell PS，Parkin RK，Kroh EM，et al. Circulating MiRNAs as stable blood-based markers for cancer detection [J]. Proc Natl Acad Sci USA，2008，105（30）：10513-10518.
[19] 杨丽华，董琢，龚朝辉，等.细胞外微RNA：一种新型的肺癌分子生物标志物[J].遗传，2012，34（6）：651-658.
[20] 蔡晓懿，夏正坤，张春妮，等.血清miRNAs在局灶节段性肾小球硬化及微小病变性肾病中的表达[J].临床儿科杂志，2013，31（4）：328-330.