ArticleExperimental and therapeutic medicine2020
lncRNA MIAT increases cell viability, migration, EMT and ECM production in age-related cataracts by regulating the miR-181a/CTGF/ERK signaling pathway.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- A comprehensive investigation of identifying miRNA biomarkers and their potential role in age-related cataract by meta-analysis and bioinformatics analysis.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025Pooled it
- Expression and function of CCN2-derived circRNAs in chondrocytes.Journal of cell communication and signaling · 2023Article
- Article
- The Role ofInternational journal of biological sciences · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related cataract (ARC) is a common cause of blindness in elderly individuals. Long non-coding RNA (lncRNA) myocardial infarction associated transcript (MIAT) has been reported to participate in various biological processes in a number of diseases; however, the biological mechanism underlying MIAT during ARC is not completely understood. The expression levels of MIAT, microRNA (miR)-181a and connective tissue growth factor (CTGF) were measured by reverse transcription-quantitative PCR. The protein expression levels of CTGF, α-smooth muscle actin, fibronectin, collagen type I, ERK, phosphorylated (p)-ERK, mitogen-activated protein kinase (MEK), and p-MEK were detected by western blotting. Cell viability and migration were assessed using MTT and Transwell assays, respectively. Moreover, a dual-luciferase reporter assay was performed to investigate the interaction between miR-181a and MIAT or CTGF. MIAT and CTGF were upregulated, while miR-181a was significantly downregulated in ARC tissues compared with normal tissues. MIAT or CTGF knockdown decreased cell viability, migration, epithelial-mesenchymal transition and extracellular matrix production in TGF-β2-treated SRA01/04 cells. It was hypothesized that miR-181a may be sponged by MIAT and may target CTGF. Furthermore, the miR-181a inhibitor reversed the inhibitory effect of MIAT knockdown on the progression of TGF-β2-treated SRA01/04 cells. Moreover, CTGF knockdown also reversed MIAT overexpression-mediated progression of TGF-β2-treated SRA01/04 cells. In addition, MIAT and CTGF regulated the activity of the ERK signaling pathway. The results suggested that MIAT may regulate the progression of ARC via the miR-181a/CTGF/ERK signaling pathway, which may serve as a novel therapeutic target for ARC.
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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.