Table 2

The role of long non-coding RNAs (lncRNAs) in various kinds of visual impairment

Official symbolAlso known asGenomic locationRelated diseaseAlterationFunction
CRNDECRNDEP; PNAS-108; lincIRX5; LINC00180; NCRNA0018016q12.2Uveal
Melanoma
Dys
regulation
CRNDE were associated with good prognosis via epigenetic mechanisms, particularly through histone methylation or demethylation by the PRC2 or CoREST complexes.
LINC-RORROR; lincRNA-RoR18q21.31Uveal
melanoma
UpregulationLINC-ROR acts as an oncogenic lncRNA, activating the TESC promoter by repelling the histone G9A methyltransferase and promoting the release of histone H3K9. Suppression of ROR could reduce tumour growth and metastasis as reported.
BANCRLINC00586Chr 9RetinoblastomaUp
regulation
BANCR is overexpressed and associated with tumour size, choroidal invasion, and optic nerve invasion. Moreover, patients with high levels of lncRNA BANCR expression had poorer survival than those with lower levels of lncRNA BANCR expression.
PISRT1NCRNA001953q23BPESDys
regulation
PISRT1 deletion could be involved in FOXL2 regulation and constitutes the smallest deletion described in a female with BPES.
LINC00237NCRNA0023720p11.23MOMO
syndrome
LINC00237 was expressed in lymphocytes of control individuals while normal transcripts were absent in lymphocytes of our MOMO patient.
MALAT1HCN; NEAT2; PRO2853; mascRNA; LINC00047; NCRNA0004711q13.1Diabetic
retinopathy
Up
regulation
MALAT1 downregulation could obviously ameliorate DR by functioning as a competing endogenous RNA in the regulation of VEGF levels through miR-150-5p.
Retinopathy of prematurityUp
regulation
Knocking down of MALAT1 tips the balance from a proliferative to a migratory endothelial cell phenotype in vitro, and its genetic deletion restrains vascular growth in vivo.
Retinal
neurodegeneration
Up
regulation
MALAT1 knockdown reduces reactive gliosis, Müller cell activation, and RGC survival in vivo and in vitro. MALAT1 regulates Müller and RGC function through CREB signalling.
Proliferative vitreoretinopathyUp
regulation
MALAT1 related to RPE proliferation and migration, promotion of ERM formation, and PVR pathogenesis. MALAT1 upregulation appeared in the cellular and plasma fraction of peripheral blood in PVR patients as well and obviously reduced after PVR operation.
rs9362054Chr 6Diabetic
retinopathy
Dys
regulation
Top signal of DR susceptibility loci.
Vax2osVas2os; Vax2os1; Vax2os26 C3Ocular
neovascularisation
Up
regulation
Vax2os significantly upregulated in the aqueous humour of patients with CNV AMD and murine ocular neovascular models.
NR_033585Corneal
neovascularisation
Up
regulation
The lncRNA NR_033585 was significantly upregulated in vascularised corneas and presented a similar expression pattern as pro-angiogenic factors.
Chr8:129102060–129109035Corneal
neovascularisation
Down
regulation
lincRNA chr8:129102060–129109035 reverse strand was found to be markedly downregulated in vascularised corneas.
CDKN2B-AS1ANRIL; p15AS; PCAT12; CDKN2BAS; CDKN2B-AS; NCRNA000899p21.3GlaucomaDys
regulation
CDKN2B-AS1 is the genetic susceptibility locus for glaucoma, influencing the nearby CDKN2A and CDKN2B genes via regulatory mechanisms, which can influence cell proliferation and senescence.
LOXL1-AS115q24.1Exfoliation
glaucoma
Dys
regulation
LOXL1-AS1 manipulates the activity of promoter in LOXL1 region.
MIATRNCR2; GOMAFU; C22orf35; LINC00066; NCRNA00066; lncRNA-MIAT22q12.1Age-related
cataract
Up
regulation
MIAT knockdown could repress TNF-α-induced abnormal proliferation and migration of HLECs, by acting as a ceRNA and formed a feedback loop with Akt and miR-150-5p.
MEG3GTL2; FP504; prebp1; PRO0518; PRO2160; LINC00023; NCRNA0002314q32Diabetic
retinopathy
Down
regulation
MEG3 knockdown aggravates retinal vessel dysfunction in vivo, and also regulates retinal endothelial cell proliferation, migration and tube formation in vitro.
RetinoblastomaDown
regulation
MEG3 is significantly downregulated and that the reduced expression is associated with a poor prognosis among patients with retinoblastoma.
  • AMD, age-related macular degeneration; BPES, blepharophimosis, ptosis and epicanthus inversus syndrome; CNV, choroidal neovascularisation; HLEC, human lens epithelial cell; RPE, retinal pigmented epithelium; TNF-α, tumour necrosis factor α; VEGF, vascular endothelial growth factor.