MATERIALS AND METHODS: Rhesus macaque choroid retinal endothelial cell line (RF/6A) cells were cultivated in normal glucose (NG) and high glucose (HG) conditions. The mRNA expression of miR-424 and Cyclin D1 (CCND1) was quantified using qPCR, and the protein quantity of CCND1 was detected using Western Blot. miR-424 mimics, miR-424 inhibitors, miR-424 inhibitor+ siRNA-CCND1 or vehicle molecules were transfected into RF/6A cells. MTT test was used to assess cell proliferation, and flow cytometric analysis was used to assess cell cycle. The interaction between miR-424 and CCND1 was predicted using bioinformatics and validated using dual luciferase reporter analysis.
RESULTS: miR-424 was up-regulated, and cell viability was reduced in HG compared to NG. By reversing the expression of miR-424 in certain situations, the phenotypes can be changed. CCND1 has been identified as a miR-424 target gene, and it may be regulated at the transcriptional and translational levels. Manipulation of silencing CCND1 can counteract the effect of transfecting miR-424 inhibitor into RF/6A cells under HG such as proliferation stimulation.
CONCLUSIONS: Our findings indicate that miR-424 plays an important role in hyperglycemia induced ARPE-19 cells damage, and it could be a new therapeutic target for DR by preventing retinal vascular cells from HG-induced injury.
PURPOSE: This study evaluated differences of TPC and TNF-α concentrations in tears at different severity of NPDR among participants with diabetes in comparison with normal participants.
METHODS: A total of 75 participants were categorized based on Early Treatment for Diabetic Retinopathy Study scale, with 15 participants representing each group, namely, normal, diabetes without retinopathy, mild NPDR, moderate NPDR, and severe NPDR. All participants were screened using McMonnies questionnaire. Refraction was conducted subjectively. Visual acuity was measured using a LogMAR chart. Twenty-five microliters of basal tears was collected using glass capillary tubes. Total protein concentration and TNF-α concentrations were determined using Bradford assay and enzyme-linked immunosorbent assay, respectively.
RESULTS: Mean ± SD age of participants (n = 75) was 57.88 ± 4.71 years, and participants scored equally in McMonnies questionnaire (P = .90). Mean visual acuity was significantly different in severe NPDR (P = .003). Mean tear TPC was significantly lower, and mean tear TNF-α concentration was significantly higher in moderate and severe NPDR (P < .001). Mean ± SD tear TPC and TNF-α concentrations for normal were 7.10 ± 1.53 and 1.39 ± 0.24 pg/mL; for diabetes without retinopathy, 6.37 ± 1.65 and 1.53 ± 0.27 pg/mL; for mild NPDR, 6.32 ± 2.05 and 1.60 ± 0.21 pg/mL; for moderate NPDR, 3.88 ± 1.38 and 1.99 ± 0.05 pg/mL; and for severe NPDR, 3.64 ± 1.26 and 2.21 ± 0.04 pg/mL, respectively. Tear TPC and TNF-α concentrations were significantly correlated (r = -0.50, P < .0001). Visual acuity was significantly correlated with tear TPC (r = -0.236, P = .04) and TNF-α concentrations (r = 0.432, P < .0001).
CONCLUSIONS: This cross-sectional study identified differences in tear TPC and TNF-α concentrations with increasing severity of NPDR.
OBJECTIVES: To assess the effects of topical non-steroidal anti-inflammatory drugs (NSAIDs) for diabetic cystoid macular oedema (CMO).
SEARCH METHODS: We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (2014, Issue 12), Ovid MEDLINE, Ovid MEDLINE In-Process and Other Non-Indexed Citations, Ovid MEDLINE Daily, Ovid OLDMEDLINE (January 1946 to January 2015), EMBASE (January 1980 to January 2015), Latin American and Caribbean Health Sciences Literature Database (LILACS) (January 1982 to January 2015), the ISRCTN registry (www.isrctn.com/editAdvancedSearch), ClinicalTrials.gov (www.clinicaltrials.gov) and the WHO International Clinical Trials Registry Platform (ICTRP) (www.who.int/ictrp/search/en). We did not use any date or language restrictions in the electronic searches for trials. We last searched the electronic databases on 12 January 2015.
SELECTION CRITERIA: Randomised controlled trials (RCTs) and quasi-RCTs investigating the effects of topically applied NSAIDs in the treatment of people with diabetic CMO aged 18 years of age or over.
DATA COLLECTION AND ANALYSIS: Two review authors independently assessed trial eligibility and screened all available titles and abstracts for inclusion. There were no discrepancies and we did not have to contact trial investigators for missing data.
MAIN RESULTS: We did not identify any RCTs matching the inclusion criteria for this review.
AUTHORS' CONCLUSIONS: The review did not identify any RCTs investigating the effects of topical NSAIDs in the treatment of diabetic CMO. Most of the studies identified through the electronic searches had been conducted to analyse the effect of topical NSAIDs for pseudophakic CMO.In the absence of high quality evidence, clinicians need to use their clinical judgement and other low level evidence, such as observational non-randomised trials, to decide whether to use topical NSAIDs in cases of diabetic CMO.More research is needed to better understand the cause of this condition and its pathophysiology. This systematic review has identified the need for well designed, adequately powered RCTs to assess possible beneficial and adverse effects of topical NSAIDs in people with diabetic CMO. Future trials should aim to include a large sample size with an adequate follow-up period of up to one year.