ArticleInternational journal of clinical and experimental pathology2017
The impact of miR-26b on retinal pigment epithelium cells in rhegmatogenous retinal detachment model.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Rs1894720 polymorphism is associated with the risk of age-related cataract by regulating the proliferation of epithelial cells in the lens via the signalling pathway of MIAT/miR-26b/BCL2L2.Archives of medical science : AMS · 2022Article
- The Impact of miRNAs in Health and Disease of Retinal Pigment Epithelium.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhegmatogenous retinal detachment (RRD) is a type of blind eye disease that seriously affects the physical and mental health. The early pathological changes are closely related to the migration of retinal pigment epithelium (RPE) cells to the vitreous body. It was showed miR-26b plays an important role in regulating lens epithelial cell growth and proliferation. However, the expression and role of miR-26b in RPE from RRD is still unclear. Rabbit RRD model was established. RPE cells were isolated and cultivated. MiR-26b inhibitor was transfected to RPE cells from model group. MiR-26b expression was tested by Real-time PCR. RPE cell proliferation was evaluated by MTT assay. Ki-67 and PCNA expressions were detected by Western blot. Caspase 3 activity was measured by the kit. RPE cell invasion was determined by Transwell assay. MiR-26b significantly increased in RPE cells from model group. It obviously promoted RPE cell proliferation and invasion, suppressed Caspase 3 activity, and upregulated Ki-67 and PCNA expression compared with control (P < 0.05). MiR-26b inhibitor transfection markedly restrained RPE cell proliferation and invasion, enhanced Caspase 3 activity, and inhibited Ki-67 and PCNA levels compared with model group (P < 0.05). MiR-26b expression was upregulated in RRD. Downregulation of miR-26b can postpone the occurrence and development of RRD through inhibiting Ki-67 and PCNA, regulating cell apoptosis, and restraining RPE cell proliferation and invasion.
Indexed as
Identifiers
31966666PMC6965422W3005810151What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.