Related Experiment Video
Updated: Aug 5, 2026

Engineering Antiviral Agents via Surface Plasmon Resonance
Published on: June 14, 2022
Caveola and Its Resident Proteins, Caveolin-1 and -2, Play Critical Roles in the Pathogenesis of nAMD and PCV
Richard Ming Chuan Yu1, Gokce Oguz2,3,4, Nai Yang Fu5
1Retina Research Group, Singapore Eye Research Institute, Singapore, Republic of Singapore.
Purpose:
The purpose of this study was to investigate cellular and molecular mechanisms underlying neovascular age-related macular degeneration (nAMD) and polypoidal choroidal vasculopathy (PCV) via single-cell RNA sequencing (scRNA-seq), then focusing on caveolae-resident proteins based on identified negatively enriched caveolae via Gene Set Enrichment Analysis (GSEA).
Methods:
Peripheral blood mononuclear cells (PBMCs) from patients with nAMD/PCV (n = 10) and healthy controls (n = 9) were collected. A total of 22,593 high-quality monocytes were analyzed for differentially expressed genes (DEGs) and GSEA. The key finding of negatively enriched caveola was recapitulated by in vitro mRNA transfections in THP-1 monocytes and human umbilical vein endothelial cells (HUVECs), followed by validation using qPCR. Functional assays and cytokine profiling were also performed.
Results:
A total of 122 significant pathways was identified from WikiPathways, Reactome, Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Ontology. GSEA revealed significant negative enrichment of caveola in classical monocytes of PCV (NES = -1.769, P = 0.001, q = 0.026). Cytokine/chemokine profiling revealed that Caveolin (CAV)1/2-overexpressing monocytes secreted markedly higher levels of several proinflammatory mediators, including IL-1β, IL-2, IL-8, IL-17, TNF-α, PDGF-BB, and MIP-1α/β. CAV1 or CAV2 overexpression in THP-1 cells increased monocyte adhesion but inhibited transendothelial migration. In HUVECs, their overexpression induced moderate cytokine profiles, including downregulation of RANTES (CCL5), IL-10, and VEGF, and upregulation of IL-6 and MIP-1α. CAV1/2 overexpression also significantly inhibited tube formation, whereas knockdown of CAV1 or CAV2 enhanced tube formation.
Conclusions:
Caveolins appear to contribute to the pathogenesis of nAMD and PCV as modulators of inflammation and vascular function. Enhanced CAV1/2 expression in endothelial cells attenuates angiogenic activity, indicating a potential therapeutic strategy.
More Related Videos
06:03Use of Viral Entry Assays and Molecular Docking Analysis for the Identification of Antiviral Candidates against Coxsackievirus A16
Published on: July 15, 2019
09:13Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy
Published on: November 1, 2011
Related Concept Videos
Cystic Fibrosis: Pathogenesis
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation, but...
Clathrin Coated Vesicles
Coat Assembly and GTPases
Coat assembly depends on the local availability of phosphatidylinositol phosphates or PIPs and GTP-binding proteins. Adaptor proteins, which link the coat proteins to the membrane, bind to these PIPs and play a crucial role in controlling...
Pinching-off of Coated Vesicles
Regulation of Nuclear Protein Sorting
Overview of Secretory Vesicles
Various proteins regulate the aggregation of molecules inside the secretory vesicles. Chromogranins...