ArticleInternational journal of ophthalmology2021
LRG1 promotes epithelial-mesenchymal transition of retinal pigment epithelium cells by activating NOX4.
Article in International journal of ophthalmology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- LRG1 as a Potential Therapeutic Target in Atherosclerosis: Mechanistic Basis and Current Evidence.Cells · 2026Review
- The critical role of LRG1 in pathological fibrosis.Journal of molecular medicine (Berlin, Germany) · 2025Review
- The disruptive role of LRG1 on the vasculature and perivascular microenvironment.Frontiers in cardiovascular medicine · 2024Review
- Metformin regulates the LIN28B‑mediated JNK/STAT3 signaling pathway through miR‑140‑3p in subretinal fibrosis.Experimental and therapeutic medicine · 2023Article
- Role of Oxidative Stress in Ocular Diseases: A Balancing Act.Metabolites · 2023Review
- Leucine rich alpha-2-glycoprotein 1 (Lrg1) silencing protects against sepsis-mediated brain injury by inhibiting transforming growth factor beta1 (TGFβ1)/SMAD signaling pathway.Bioengineered · 2022Article
- LRG1 as a novel therapeutic target in eye disease.Eye (London, England) · 2022Review
- The role of leucine-rich alpha-2-glycoprotein-1 in proliferation, migration, and invasion of tumors.Journal of cancer research and clinical oncology · 2022Review
- LRG1: an emerging player in disease pathogenesis.Journal of biomedical science · 2022Review
- Research Progress on Leucine-Rich Alpha-2 Glycoprotein 1: A Review.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the effect of leucine-rich-alpha-2-glycoprotein 1 (LRG1) on epithelial-mesenchymal transition (EMT) in retinal pigment epithelium (RPE) cells, and to explore the role of NADPH oxidase 4 (NOX4).
methodsRPE cells (ARPE-19 cell line) were treated with transforming growth factor-β1 (TGF-β1) to induce EMT. Changes of the mRNA and protein expression levels of LRG1 were tested in the TGF-β1 treated cells. The recombinant human LRG1 protein (rLRG1) and siRNA of LRG1 were used to establish accumulation of exogenous LRG1 model and the down-regulation of LRG1 model in ARPE-19 cells respectively, and to detect EMT-related markers including fibronectin, α-smooth muscle actin (α-SMA) and zonula occludens-1 (ZO-1). The mRNA and protein expression level of NOX4 were measured according to the above treatments. VAS2870 was used as a NOX4 inhibitor in rLRG1-treated cells. EMT-related markers were detected to verify the effect of NOX4 in the process of EMT.
resultsTGF-β1 promoted the expression of LRG1 at both the mRNA and protein levels during the process of EMT which showed the up-regulation of fibronectin and α-SMA, as well as the down-regulation of ZO-1. Furthermore, the rLRG1 promoted EMT of ARPE-19 cells, which manifested high levels of fibronectin and α-SMA and low level of ZO-1, whereas knockdown of LRG1 prevented EMT by decreasing the expressions of fibronectin and α-SMA and increasing the expression of ZO-1 in ARPE-19 cells. Besides, the rLRG1 activated and LRG1 siRNA suppressed NOX4 expression. EMT was inhibited when VAS2870 was used in the rLRG1-treated cells.
conclusionThese results for the first time demonstrate that LRG1 promotes EMT of RPE cells by activating NOX4, which may provide a novel direction to explore the mechanisms of subretinal fibrosis.
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