miR-195 regulates SIRT1-mediated changes in diabetic retinopathy

Mortuza, Rokhsana; Feng, Biao; Chakrabarti, Subrata

doi:10.1007/s00125-014-3197-9

Cited by 135 publications

(107 citation statements)

References 49 publications

Supporting

Mentioning

103

Contrasting

Order By: Relevance

“…These results are also in keeping with previous studies by other investigators who have shown that UnAG protects microvascular endothelial cells from apoptosis through SIRT1 (10). Furthermore, in the endothelial cells and in other organs affected by chronic diabetes complications, accelerated senescence and SIRT1 downregulation, at least in part mediated by other miRs, have been demonstrated (11,12). miR alterations play important regulatory roles in several, if not all, physiological and pathological processes (13).…”

supporting

confidence: 91%

Unacylated Ghrelin: A Gut-Limb Connection

Chakrabarti

2015

Diabetes

Self Cite

View full text Add to dashboard Cite

supporting

confidence: 91%

Unacylated Ghrelin: A Gut-Limb Connection

Chakrabarti

2015

Diabetes

Self Cite

View full text Add to dashboard Cite

“…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. Moreover, recent studies also showed that high glucose concentration could elevate miR-195 expression [42,43].…”

Section: Discussionmentioning

confidence: 99%

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

Sayilar¹

2016

J Diabetes Metab

View full text Add to dashboard Cite

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.

show abstract

“…As highly conserved, short non-coding RNAs (21-25 nucleotides in length), miRNAs negatively regulate gene expression at the post-transcriptional level by binding to the 3′ untranslated region (3′-UTR) of target mRNA, leading to its degradation or translational repression [17]. Several miRNAs regulate SIRT1 in various disease conditions, including diabetic retinopathy [18][19][20]. However, no studies have focused on the regulation of SIRT1 in the cellular metabolic memory of diabetic retinopathy.…”

Section: Introductionmentioning

confidence: 99%

miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway

Zhao

et al. 2015

Diabetologia

View full text Add to dashboard Cite

Aims/hypothesis The mechanisms underlying the cellular metabolic memory induced by high glucose remain unclear. Here, we sought to determine the effects of microRNAs (miRNAs) on metabolic memory in diabetic retinopathy. Methods The miRNA microarray was used to examine human retinal endothelial cells (HRECs) following exposure to normal glucose (N) or high glucose (H) for 1 week or transient H for 2 days followed by N for another 5 days (H→N). Levels of sirtuin 1 (SIRT1) and acetylated-nuclear factor κB (Ac-NF-κB) were examined following transfection with miR-23b-3p inhibitor or with SIRT1 small interfering (si)RNA in the H→N group, and the apoptotic HRECs were determined by flow cytometry. Retinal tissues from diabetic rats were similarly studied following intravitreal injection of miR-23b-3p inhibitor. Chromatin immunoprecipitation (ChIP) analysis was performed to detect binding of NF-κB p65 to the potential binding site of the miR-23b-27b-24-1 gene promoter in HRECs. Results High glucose increased miR-23b-3p expression, even after the return to normal glucose. Luciferase assays identified SIRT1 as a target mRNA of miR-23b-3p. Reduced miR-23b-3p expression inhibited Ac-NF-κB expression by rescuing SIRT1 expression and also relieved the effect of metabolic memory induced by high glucose in HRECs. The results were confirmed in the retina using a diabetic rat model of metabolic memory. High glucose facilitated the recruitment of NF-κB p65 and promoted transcription of the miR-23b-27b-24-1 gene, which can be suppressed by decreasing miR-23b-3p expression. Conclusions/interpretation These studies identify a novel mechanism whereby miR-23b-3p regulates high-glucoseinduced cellular metabolic memory in diabetic retinopathy through a SIRT1-dependent signalling pathway.

show abstract

miR-195 regulates SIRT1-mediated changes in diabetic retinopathy

Abstract: These studies identified a novel mechanism whereby miR-195 regulates SIRT1-mediated tissue damage in diabetic retinopathy.

Cited by 135 publications

References 49 publications

Unacylated Ghrelin: A Gut-Limb Connection

Unacylated Ghrelin: A Gut-Limb Connection

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

miR-23b-3p induces the cellular metabolic memory of high glucose in diabetic retinopathy through a SIRT1-dependent signalling pathway

Contact Info

Product

Resources

About