Abated microRNA-195 expression protected mesangial cells from apoptosis in early diabetic renal injury in mice

Chen, Yu Qiang; Wang, Xiao X.; Yao, Xing M.; Zhang, Dong L.; Yang, Xu; Tian, Shou F.; Wang, Nian S.

doi:10.5301/jn.5000034

Cited by 66 publications

(44 citation statements)

References 26 publications

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“…These findings suggested that miR-195 might mediate podocyte apoptosis in DN. In line with this study, miR-195 was observed to be increased not only in STZ-induced type 1 diabetic mice but also in high glucose cultured MMCs, followed by enhanced apoptosis of MMCs [43]. …”

Section: Upregulated Mirnas In Dnsupporting

confidence: 73%

The Role of MicroRNAs in Diabetic Nephropathy

Kong

Zhou

et al. 2014

Journal of Diabetes Research

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Diabetic nephropathy (DN), as one of the chronic complications of diabetes, is the major cause of end-stage renal disease. However, the pathogenesis of this disease is not fully understood. In recent years, research on microRNAs (miRNAs) has become a hotspot because of their critical role in regulating posttranscriptional levels of protein-coding genes that may serve as key pathogenic factors in diseases. Several miRNAs were found to participate in the pathogenesis of DN, while others showed renal protective effects. Therefore, targeting miRNAs that are involved in DN may have a good prospect in the treatment of the disease. The aim of this review is to summarize DN-related miRNAs and provide potential targets for diagnostic strategies and therapeutic intervention.

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Section: Upregulated Mirnas In Dnsupporting

confidence: 73%

The Role of MicroRNAs in Diabetic Nephropathy

Kong

Zhou

et al. 2014

Journal of Diabetes Research

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“…A recent study showed a reduction in miR-195 in the kidney of STZ-induced type 1 diabetic mice [31]. However, upregulation of miR-195 was revealed in liver in a rat model of spontaneous type 2 diabetes [32] and in retinas of STZ-induced diabetic rats [33].…”

Section: Discussionmentioning

confidence: 99%

Silencing of miR-195 reduces diabetic cardiomyopathy in C57BL/6 mice

et al. 2015

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Aims/hypothesis MicroRNAs (miRs) have been suggested as potential therapeutic targets for heart diseases. Inhibition of miR-195 prevents apoptosis in cardiomyocytes stimulated with palmitate and transgenic overexpression of miR-195 induces cardiac hypertrophy and heart failure. We investigated whether silencing of miR-195 reduces diabetic cardiomyopathy in a mouse model of streptozotocin (STZ)-induced type 1 diabetes. Methods Type 1 diabetes was induced in C57BL/6 mice (male, 2 months old) by injections of STZ. Results MiR-195 expression was increased and levels of its target proteins (B cell leukaemia/lymphoma 2 and sirtuin 1) were decreased in STZ-induced type 1 and db/db type 2 diabetic mouse hearts. Systemically delivering an anti-miR-195 construct knocked down miR-195 expression in the heart, reduced caspase-3 activity, decreased oxidative stress, attenuated myocardial hypertrophy and improved myocardial function in STZ-induced mice with a concurrent upregulation of B cell leukaemia/lymphoma 2 and sirtuin 1. Diabetes reduced myocardial capillary density and decreased maximal coronary blood flow in mice. Knockdown of miR-195 increased myocardial capillary density and improved maximal coronary blood flow in diabetic mice. Upregulation of miR-195 sufficiently induced apoptosis in cardiomyocytes and attenuated the angiogenesis of cardiac endothelial cells in vitro. Furthermore, inhibition of miR-195 prevented apoptosis in cardiac endothelial cells in response to NEFA, an important feature of diabetes. Conclusions/interpretation Therapeutic silencing of miR-195 reduces myocardial hypertrophy and improves coronary blood flow and myocardial function in diabetes, at least in part by reducing oxidative damage, inhibiting apoptosis and promoting angiogenesis. Thus, miR-195 may represent an alternative therapeutic target for diabetic heart diseases.

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“…miR-195, a member of the miRNA family that play a role in DN etiology and physiology, show antiapoptotic features due to its down-regulation. Chen et al's [41] rat model study showed that in early stages of DN, miR-195 expression decreased, was along with a reverse association between miR-195 expression level and glomerular diameter. Higher than control urinary and plasma miR-195 expression levels in stage 3 and stage 5 CKD patients, respectively in the present study can be explained by the furthering of the renal parenchymal damage and primarily renal cortex damage in relation with miR-195 down-regulation; shrinking in the glomeruli; fibrosis; and increased apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Biomarker Potential of Urine miR-451 at Different Stages of Diabetic Nephropathy

Sayilar¹

2016

J Diabetes Metab

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Aims: To evaluate the potential of urinary miR-451 as a biomarker at different stages of diabetic nephropathy.Methods: A total of 45 subjects having stage 3 chronic kidney disease (n=15) or stage 5 chronic kidney disease (n=15) and 15 healthy volunteers were included. Data on patient demographics, laboratory findings [creatinine, estimated glomerular filtration rate, urinary protein excretion] target genes and functions of the selected MicroRNAs associated with diabetic nephropathy and fold differences in the level of MicroRNA expression in blood and urine and the correlation of urine and plasma MicroRNA expression with estimated glomerular filtration rate were recorded.

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Abated microRNA-195 expression protected mesangial cells from apoptosis in early diabetic renal injury in mice

Abstract: These results demonstrated that the abated microRNA-195 expression protected mesangial cells from apoptosis, suggesting that the antiapoptosis in a microRNA-regulated manner may play an important role in the early stages of diabetic nephropathy.

Cited by 66 publications

References 26 publications

The Role of MicroRNAs in Diabetic Nephropathy

The Role of MicroRNAs in Diabetic Nephropathy

Silencing of miR-195 reduces diabetic cardiomyopathy in C57BL/6 mice

Biomarker Potential of Urine miR-451 at Different Stages of Diabetic Nephropathy

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