ArticleMolecular medicine (Cambridge, Mass.)2012
Implication of the miR-184 and miR-204 competitive RNA network in control of mouse secondary cataract.
Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Participation of Lens Proteins and miRs in Traumatic and Inheritance Cataract: A Review on Diagnostic and Therapeutic Approaches for Cataract Management.Current pharmaceutical biotechnology · 2025Review
- miR-26 Deficiency Causes Alterations in Lens Transcriptome and Results in Adult-Onset Cataract.Investigative ophthalmology & visual science · 2024Article
- miR-26 deficiency causes alterations in lens transcriptome and results in adult-onset cataract.bioRxiv : the preprint server for biology · 2024Article
- microRNA-184 in the landscape of human malignancies: a review to roles and clinical significance.Cell death discovery · 2023Review
- Development of Electrochemical Biosensor for miR204-Based Cancer Diagnosis.Interdisciplinary sciences, computational life sciences · 2022Article
- TRPM3_miR-204: a complex locus for eye development and disease.Human genomics · 2020Review
- MicroRNA-486-5p suppresses TGF-β2-induced proliferation, invasion and epithelial-mesenchymal transition of lens epithelial cells by targeting Smad2.Journal of biosciences · 2017Article
- Transcriptome-wide Investigation of mRNA/circRNA in miR-184 and Its r.57c > u Mutant Type Treatment of Human Lens Epithelial Cells.Molecular therapy. Nucleic acids · 2017Article
- Expression of lens-related microRNAs in transparent infant lenses and congenital cataract.International journal of ophthalmology · 2017Article
- miR-184 exhibits angiostatic properties via regulation of Akt and VEGF signaling pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Autophagy and Macropinocytosis: Keeping an Eye on the Corneal/Limbal Epithelia.Investigative ophthalmology & visual science · 2017Review
- MicroRNAs: new players in cataract.American journal of translational research · 2017Review
- MicroRNAs that target RGS5.Iranian journal of basic medical sciences · 2015Article
- Expression of the microRNAs hsa-miR-15a and hsa-miR-16-1 in lens epithelial cells of patients with age-related cataract.International journal of clinical and experimental medicine · 2015Article
- MiRNA-26b inhibits the proliferation, migration, and epithelial-mesenchymal transition of lens epithelial cells.Molecular and cellular biochemistry · 2014Article
- Non-coding RNAs in the development of sensory organs and related diseases.Cellular and molecular life sciences : CMLS · 2013Review
- Pax6 regulates gene expression in the vertebrate lens through miR-204.PLoS genetics · 2013Article
- miR-204 targeting of Ankrd13A controls both mesenchymal neural crest and lens cell migration.PloS one · 2013Article
- From cellular senescence to age-associated diseases: the miRNA connection.Longevity & healthspan · 2012Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
The high recurrence rate of secondary cataract (SC) is caused by the intrinsic differentiation activity of residual lens epithelial cells after extra-capsular lens removal. The objective of this study was to identify changes in the microRNA (miRNA) expression profile during mouse SC formation and to selectively manipulate miRNA expression for potential therapeutic intervention. To model SC, mouse cataract surgery was performed and temporal changes in the miRNA expression pattern were determined by microarray analysis. To study the potential SC counterregulative effect of miRNAs, a lens capsular bag in vitro model was used. Within the first 3 wks after cataract surgery, microarray analysis demonstrated SC-associated expression pattern changes of 55 miRNAs. Of the identified miRNAs, miR-184 and miR-204 were chosen for further investigations. Manipulation of miRNA expression by the miR-184 inhibitor (anti-miR-184) and the precursor miRNA for miR-204 (pre-miR-204) attenuated SC-associated expansion and migration of lens epithelial cells and signs of epithelial to mesenchymal transition such as α-smooth muscle actin expression. In addition, pre-miR-204 attenuated SC-associated expression of the transcription factor Meis homeobox 2 (MEIS2). Examination of miRNA target binding sites for miR-184 and miR-204 revealed an extensive range of predicted target mRNA sequences that were also a target to a complex network of other SC-associated miRNAs with possible opposing functions. The identification of the SC-specific miRNA expression pattern together with the observed in vitro attenuation of SC by anti-miR-184 and pre-miR-204 suggest that miR-184 and miR-204 play a significant role in the control of SC formation in mice that is most likely regulated by a complex competitive RNA network.
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Registered trials
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