Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Self-polymerized Polyphenol-based Platform for the Management of Dry Eye Pathogenesis

ABSTRACT: A polyphenol-based eye drop is developed via the self-polymerization of rosmarinic acid in the presence hyaluronic acid, followed by co-assembly with cerium ions to afford monodispersed RHC NPs. To enhance the ocular retention efficiency, thiol groups are further decorated on NPs (termed as s-RHC NPs). In two mouse models of DED, topical administration of s-RHC NPs leads to comprehensive relief of symptoms, including inflammatory response suppression, corneal epithelial defect repair, and tear secretion recovery.

ORGANISM(S): Homo Sapiens

SUBMITTER: Yin Wang

PROVIDER: PXD071300 | iProX | Thu Nov 27 00:00:00 GMT 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Self-polymerized polyphenol-based platform for the management of dry eye pathogenesis.

Wang Zixin Z Lv Zeen Z Ge Yuxuan Y Xue Ruiyang R Wu Fang F Han Haijie H Wang Yin Y

Nature communications 20260318 1

The management of ocular surface inflammation, particularly in conditions like dry eye disease (DED), remains challenging due to multiple pathogenic causes and ocular barriers. Traditional eye drops usually provide transient and partial symptom relief, necessitating combined therapies to break the vicious cycle of oxidative stress and inflammation. To surmount these limitations, a polyphenol-based eye drop is developed via the self-polymerization of rosmarinic acid in the presence of hyaluronic ...[more]

PMID: 41851101

Similar Datasets

A Cationic Nanoemulsion Preserves Corneal Barrier Function and Meibomian Gland Integrity in Contact Lens–Related Dry Eye

Project description:Purpose: To establish a clinically relevant mouse model of contact lens–related dry eye (CLDE) and evaluate the therapeutic effects and potential mechanisms of the cationic nanoemulsion Cationorm®. Methods: CLDE was induced by combined benzalkonium chloride (BAC) exposure and daily contact lens wear. After model establishment, mice were treated with normal saline, hyaluronic acid (HA), or Cationorm®. Tear film stability, tear secretion, and corneal epithelial damage were assessed using tear breakup time, phenol red thread test, and corneal fluorescein staining. Corneal and meibomian gland morphology were evaluated by histology, apoptosis was assessed by TUNEL staining, and barrier- and inflammation-related gene expression was analyzed by RT-qPCR. RNA sequencing was performed to explore treatment-associated molecular pathways. Results: The BAC+CL model induced tear film instability, reduced tear secretion, corneal epithelial damage, barrier-related gene dysregulation, and ocular surface inflammation. Cationorm® significantly prolonged tear breakup time compared with saline and HA and partially improved tear secretion. Cationorm® reduced corneal epithelial damage, improved corneal epithelial morphology, and increased the expression of barrier-related genes, including Zo1 and Occludin. Inflammatory markers, including Il1b, Tnfa, and Mmp9, were reduced after Cationorm® treatment. Cationorm® also reduced apoptosis in the cornea and meibomian gland and preserved meibomian gland structure. Transcriptomic analysis revealed enrichment of epithelial junction–related and immune-related pathways associated with Cationorm® treatment. Conclusions: Cationorm® improves ocular surface abnormalities in a dual-hit CLDE mouse model through coordinated effects on tear film stability, corneal epithelial integrity, inflammation, apoptosis, and meibomian gland structure. These findings support its potential as a multi-target therapeutic strategy for CLDE.

2026-06-25 | GSE335869 | GEO

Lacripep promotes corneal regeneration in autoimmune mediated dry eye disease

Project description:Corneal architecture is essential for vision and is greatly perturbed by the absence of tears due to the highly prevalent disorder dry eye. With no regenerative therapies available, pathological alterations of the ocular surface in response to dryness, including persistent epithelial defects and poor wound healing, result in lifelong morbidity. Here, using a mouse model of aqueous-deficient dry eye, we reveal that topical application of the synthetic tear protein lacripep reverses the pathological outcomes of dry eye through restoring the extensive network of corneal nerves that are essential for tear secretion, barrier function, epithelial homeostasis and wound healing. Intriguingly, the restorative effects of lacripep occur despite extensive immune cell infiltration, suggesting tissue reinnervation and regeneration can be achieved under chronic inflammatory conditions. In summary, our data highlight lacripep as a first-in-class regenerative therapy for returning the cornea to a near homeostatic state in individuals who suffer from dry eye.

2022-07-18 | GSE208297 | GEO

Modeling dry eye with an air-liquid interface in corneal epithelium-on-a-chip

Project description:Dry eye syndrome (DES) is a complex ocular condition characterized by an unstable tear film and inadequate tear production, leading to tissue damage. Despite its common occurrence, there is currently no comprehensive in vitro model that accurately reproduce the cellular characteristics of DES. Here we modified a corneal epithelium-on-a-chip (CEpOC) model to recapitulate DES by subjecting HCE-T human corneal epithelial cells to an air-liquid (AL) interface stimulus. We then assessed the effects of AL stimulation both in the presence and absence of diclofenac (DCF). Transcriptomic analysis revealed distinct gene expression changes in response to AL and AL_DCF, affecting pathways related to development, epithelial structure, inflammation, and extracellular matrix remodeling. Both treatments upregulated PIEZO2, linked to corneal damage signaling, while downregulating OCLN, involved in cell-cell junctions. They increased the expression of inflammatory genes (e.g., IL6) and reduced mucin production genes (e.g., MUC16), reflecting dry eye characteristics. TGFB1, crucial for corneal wound healing, was slightly downregulated in AL_DCF, potentially affecting wound healing processes rather than reducing inflammation by DCF. Metabolomic analysis showed increased secretion of metabolites associated with cell damage and inflammation (e.g., methyl-2-oxovaleric acid, 3-methyl-2-oxobutanoic acid, lauroyl-carnitine) in response to AL and even more with AL_DCF, indicating a shift in cellular metabolism. This study showcases the utilization of AL stimulus within the CEpOC as a comprehensive approach to faithfully reproduce the cellular characteristics of DES.

2023-10-11 | GSE244787 | GEO

Human Tear using MALDI-TOF-MS for Dry Eye syndrome

Project description:Tears are a biological fluid that has diagnostic potential for ocular diseases. Extracellular vesicles (EVs), wildly detected in various biofluids including tears, are nanoparticles released by living cells and considered as promising detection sources for non-invasive liquid biopsy. Understanding the roles of tears and tear-EVs in ocular diseases such as dry eye can facilitate the studies of clinical diagnosis, which usually entails detecting such liquid objects with a rapid and effective method. In this study, we utilized a mass spectrometry based strategy to analyze peptidome/proteome profiles of tear and EVs for rapid dry eye diagnosis. Nano-sized EVs were isolated from tears of either healthy control (HC) individuals or dry eye syndrome (DES) patients, and the tear compositions were further analyzed by tracking their fingerprints with matrix-assisted laser desorption ionization/time-of-flight mass spectrometry (MALDI-TOF-MS). The fingerprints of tear-EVs could be observed in a dose-dependent manner as well as tears, allowing comparing their discriminant peaks between tears and EVs. By analyzing these peaks, the fingerprints of both tear and tear-EVs were showed to have a capability of distinguishing DES patients from HC donors, and providing an efficient way for screening potential DES biomarkers. The proposed tear and EV fingerprinting approach is expected to be a potential tool in rapid diagnosis of ocular disease and in-depth researches of pathogenesis.

2020-08-20 | PXD020217 | Pride

MSCs-encapsulated porous microparticle eye drops for autoimmune dry eye disease treatment

Project description:Dry eye disease (DED) characterizes by chronic inflammation and an unstable tear film. Stem cells have shown potential for DED treatment, but the main challenge lies in improving the effectiveness of cell delivery. Here, we developed novel eye drops for DED treatment by employing porous microcarriers with mesenchymal stem cells. The microcarriers were created by electrospraying the solution of Arginine-Glycine-Aspartic Acid (RGD) peptides-modified sodium alginate with polyethylene oxide and mesenchymal stem/stromal cells (MSCs) into the calcium chloride solution. In vitro experiments based on a hyperosmotic corneal epithelial cell model indicated that porous microcarriers encapsulated with MSCs (RGD-Alg@MSCs) demonstrated notable enhancements in cell viability, reductions in apoptosis and reactive oxygen species (ROS), and diminished expression of pro-inflammatory cytokines. In the DED model using non-obese diabetic (NOD) mice, RGD-Alg@MSCs effectively enhanced tear production, promoted corneal healing, and alleviated inflammation. Additionally, RGD-Alg@MSCs modulated the immune environment in DED by inhibiting dendritic cell (DC) activation and suppressing Th17 differentiation in vitro, effectively disrupting the inflammatory feedback loop characteristic of DED. This immune modulation strategy was further validated through in vivo experiments, confirming its therapeutic potential. Thus, the designed MSCs-encapsulated porous microcarrier system can improve stem cell delivery and DED treatment efficiency.

2025-04-23 | GSE295017 | GEO

Topical lubrication restores dry eye corneal stroma by producing reparative keratocytesacripep promotes corneal regeneration in autoimmune mediated dry eye disease (snRNA-Seq).

Project description:Topical lubrication is the most common remedy for relieving the signs and symptoms of dry eye. However, the therapeutic value of lubricating the ocular surface remains relatively unknown. Here we reveal the restorative properties of the simplest form of lubrication in a mouse model of autoimmune-mediated dry eye. We show topical treatment with PBS rescues corneal stromal architecture through restoring the basement membrane and collagen fiber alignment essential for maintaining corneal transparency. At the single cell level we show keratocytes exhibit significant plasticity under chronic injury, with continuous transition from a homeostatic to inflammatory state, and that lubrication converts these inflammatory cells to a unique reparative phenotype. We further identify IL1b-IL1R1-MAPK signaling as a key pathway driving keratocyte inflammation, and that disruption of the IL1b autocrine amplification loop by lubrication is sufficient to reprogram the inflammatory keratocytes towards the reparative state. Thus, our study underscores the regenerative potential of topical lubrication in dry eye, and reveals fibroblast-targeted therapies as a novel approach to restoring ocular surface health.

2025-01-02 | GSE272700 | GEO

Topical lubrication restores dry eye corneal stroma by producing reparative keratocytesacripep promotes corneal regeneration in autoimmune mediated dry eye disease (Bulk RNA-Seq).

2025-01-02 | GSE272701 | GEO

Investigating conjunctival immune pathways in Sjögren and non-Sjögren disease associated dry eye

Project description:This study aimed to investigate changes in immune related genes on the ocular surface of patients with different diagnoses. We compared DEGs from 21 healthy controls, 12 aqueous tear deficient (ATD), and 12 Sjögren disease dry eye using the nanostring immunology v2 panel. We identified DEGs in immune pathways relating to viral response and adaptive immunity. We did not identify DEGs in comparison of ATD vs SjD, suggesting there are no differences in the immune response on the ocular surface, despite different diagnoses.

2025-12-01 | GSE311496 | GEO

Tear lipidomics profiling reveals ocular-surface lipid remodeling associated with organelle stress in a mouse model of inflammatory dry eye disease

Project description:This study aimed to determine whether dry eye disease (DED) is accompanied by ocular-surface lipid remodeling and whether such changes converge on organelle stress–associated pathways in a mouse model of inflammatory dry eye. Tear samples were collected from mice and analyzed by LC–MS/MS–based non-targeted lipidomics using a standardized workflow for sample collection, data acquisition, and computational processing. Global differential analysis revealed extensive alterations in tear lipid composition, with a substantial number of lipid features significantly upregulated or downregulated in the dry eye group compared with healthy controls, indicating robust metabolic remodeling rather than stochastic variation. Among the significantly altered lipid species, multiple lipid classes involved in membrane homeostasis and lipid signaling were prominently dysregulated, including phospholipid and fatty acid–associated species such as PE, PC, PI, and free fatty acids, which showed coordinated changes. These lipid shifts collectively indicated disruption of lipid programs that support membrane remodeling and stress adaptation at the ocular surface, consistent with a pathological state characterized by inflammatory stress and epithelial vulnerability. Pathway enrichment analysis of differentially abundant lipids further supported this interpretation, with dysregulated lipids enriched in pathways involved in glycerophospholipid metabolism, arachidonic acid/linoleic acid metabolism, and additional stress- and inflammation-associated programs, linking tear lipid remodeling to inflammatory amplification and impaired barrier homeostasis. This dataset provides a comprehensive resource for understanding tear lipid metabolic reprogramming at the ocular surface in a mouse model of inflammatory dry eye disease.

2026-04-04 | MTBLS14217 | MetaboLights

Reduced RXRa signaling increases dry eye disease inducing gdT17 cells in the conjunctiva [Nanostring]

Project description:Purpose: To investigate the mechanism for developing dry eye disease in the Pinkie mouse strain with a loss of function RXR mutation. Methods: Measures of dry eye disease were assessed in the cornea and conjunctiva. Expression profiling by single-cell RNA sequencing (scRNA-seq)was performed to compare gene expression in conjunctival immune cells. Conjunctival immune cells were immunophenotyped by flow cytometry and confocal microscopy. Activity of RXR ligand 9-cis retinoic acid (RA) was evaluated in cultured monocytes and  T cells. Results: Compared to wild type (WT) C57BL/6, Pinkie has increased signs of dry eye disease, including corneal barrier disruption, conjunctival cornification and goblet cell loss, and corneal vascularization, opacification, and ulceration with aging. scRNA-seq of conjunctival immune cells identified  T cells as the predominant IL-17 expressing population in both strains and there is a 4-fold increased percentage of  T cells in Pinkie. Compared to WT, significantly increased expression of IL-17a and IL-17f in conventional T cells and IL-17f in  T cells was found in Pinkie. Flow cytometry and immunostaining revealed an increased number of IL-17+  T cells in Pinkie. Tear concentration of the IL-17 inducer IL-23 is significantly higher in Pinkie. 9-cis RA treatment suppresses stimulated IL-17 production by  T and stimulatory activity of monocyte supernatant on  T cell IL-17 production. Compared to WT bone marrow chimeras, Pinkie chimeras have increased IL-17+  T cells in the conjunctiva after desiccating stress and anti-IL-17 treatment suppresses dry eye induced corneal MMP-9 production/activity and conjunctival goblet cell loss. Conclusion: These findings indicate that RXR suppresses generation of dry eye disease inducing  T17 cells in the conjunctiva and identifies RXR as a potential therapeutic target in dry eye.

2022-01-04 | GSE192960 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data