Mirna Expression in Glaucomatous and TGFbeta2 Treated Lamina Cribrosa Cells

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dc.creatorLopez, Navita N.
dc.creatorRangan, Rajiv
dc.creatorClark, Abbot F.
dc.creatorTovar-Vidales, Tara
dc.creator.orcid0000-0003-3594-6560 (Clark, Abbot F.)
dc.date.accessioned2022-11-28T20:48:01Z
dc.date.available2022-11-28T20:48:01Z
dc.date.issued2021-06-08
dc.description.abstractGlaucoma is a group of optic neuropathies that leads to irreversible vision loss. The optic nerve head (ONH) is the site of initial optic nerve damage in glaucoma. ONH-derived lamina cribrosa (LC) cells synthesize extracellular matrix (ECM) proteins; however, these cells are adversely affected in glaucoma and cause detrimental changes to the ONH. LC cells respond to mechanical strain by increasing the profibrotic cytokine transforming growth factor-beta 2 (TGFbeta2) and ECM proteins. Moreover, microRNAs (miRNAs or miR) regulate ECM gene expression in different fibrotic diseases, including glaucoma. A delicate homeostatic balance between profibrotic and anti-fibrotic miRNAs may contribute to the remodeling of ONH. This study aimed to determine whether modulation of miRNAs alters the expression of ECM in human LC cells. Primary human normal and glaucoma LC cells were grown to confluency and treated with or without TGFbeta2 for 24 h. Differences in expression of miRNAs were analyzed using miRNA qPCR arrays. miRNA PCR arrays showed that the miR-29 family was significantly decreased in glaucomatous LC cell strains compared to age-matched controls. TGFbeta2 treatment downregulated the expression of multiple miRNAs, including miR-29c-3p, compared to controls in LC cells. LC cells transfected with miR-29c-3p mimics or inhibitors modulated collagen expression.
dc.description.sponsorshipThis research was funded by the Glaucoma Research Foundation (TTV) and the NIH training grant T32 AG020494 (NL).
dc.identifier.citationLopez, N. N., Rangan, R., Clark, A. F., & Tovar-Vidales, T. (2021). Mirna Expression in Glaucomatous and TGFβ2 Treated Lamina Cribrosa Cells. International journal of molecular sciences, 22(12), 6178. https://doi.org/10.3390/ijms22126178
dc.identifier.issn1422-0067
dc.identifier.issue12
dc.identifier.urihttps://hdl.handle.net/20.500.12503/31978
dc.identifier.volume22
dc.publisherMDPI
dc.relation.urihttps://doi.org/10.3390/ijms22126178
dc.rights.holder© 2021 by the authors.
dc.rights.licenseAttribution 4.0 International (CC BY 4.0)
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceInternational Journal of Molecular Sciences
dc.subjectEcm
dc.subjectLC cells
dc.subjectOnh
dc.subjectmiR-29
dc.subjectmiRNAs
dc.subjectoptic nerve head
dc.subject.meshCase-Control Studies
dc.subject.meshGene Expression Profiling
dc.subject.meshGene Expression Regulation
dc.subject.meshGlaucoma / drug therapy
dc.subject.meshGlaucoma / genetics
dc.subject.meshGlaucoma / pathology
dc.subject.meshHumans
dc.subject.meshMicroRNAs / genetics
dc.subject.meshOptic Disk / drug effects
dc.subject.meshOptic Disk / metabolism
dc.subject.meshOptic Disk / pathology
dc.subject.meshOptic Nerve Diseases / drug therapy
dc.subject.meshOptic Nerve Diseases / genetics
dc.subject.meshOptic Nerve Diseases / pathology
dc.subject.meshTransforming Growth Factor beta2 / pharmacology
dc.titleMirna Expression in Glaucomatous and TGFbeta2 Treated Lamina Cribrosa Cells
dc.typeArticle
dc.type.materialtext

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