ArticleInvestigative ophthalmology & visual science2011
Selective blockade of cytoskeletal actin remodeling reduces experimental choroidal neovascularization.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- The role of the cytoskeleton in fibrotic diseases.Frontiers in cell and developmental biology · 2024Review
- Subretinal fibrosis in neovascular age-related macular degeneration: current concepts, therapeutic avenues, and future perspectives.Cell and tissue research · 2022Review
- Microbial Signatures in The Rodent Eyes With Retinal Dysfunction and Diabetic Retinopathy.Investigative ophthalmology & visual science · 2022Article
- Complement 3a Mediates CCN2/CTGF in Human Retinal Pigment Epithelial Cells.Journal of ophthalmology · 2022Article
- Myofibroblasts: Function, Formation, and Scope of Molecular Therapies for Skin Fibrosis.Biomolecules · 2021Review
- Identification of Novel Choroidal Neovascularization-Related Genes Using Laplacian Heat Diffusion Algorithm.BioMed research international · 2021Article
- Eyeing the Extracellular Matrix in Vascular Development and Microvascular Diseases and Bridging the Divide between Vascular Mechanics and Function.International journal of molecular sciences · 2020Review
- Cysteine-rich protein 61 (CCN1) and connective tissue growth factor (CCN2) at the crosshairs of ocular neovascular and fibrovascular disease therapy.Journal of cell communication and signaling · 2013Article
- Microvascular complications and diabetic retinopathy: recent advances and future implications.Future medicinal chemistry · 2013Review
- Comparative study of laser-induced choroidal neovascularization in rats by paraffin sections, frozen sections and high-resolution optical coherence tomography.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2013Article
- New Insights into the Function of the Matricellular CCN1: an Emerging Target in Proliferative Retinopathies.Journal of ophthalmic & vision research · 2013Article
- The cell-matrix interface: a possible target for treating retinal vascular related pathologies.Journal of ophthalmic & vision research · 2012Article
- COL1A2 polymorphic markers confer an increased risk of neovascular age-related macular degeneration in a Han Chinese population.Molecular vision · 2012Article
- Microvascular modifications in diabetic retinopathy.Current diabetes reports · 2011Review
- Cell-based therapies for diabetic retinopathy.Current diabetes reports · 2011Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purposeThe efficacy of the peptide Ac-EEED on reducing cell adhesion and proliferation in vitro and choroidal neovascularization (CNV) in vivo was examined.
methodsThe peptide chimera containing the Ac-EEED sequence was chemically linked to the N terminus of the XMTM delivery peptide from the E(rns) viral surface protein. Ac-EEED or scrambled control peptide (SCRAM) was added to cultures of vascular smooth muscle cells, pericytes, endothelial cells, and fibroblasts, and adhesion, growth, and matrix production was assessed. Ac-EEED or SCRAM was injected into the vitreous of mice undergoing laser rupture of Bruch's membrane to induce CNV and lesion volume, neovascularization and lesion fibrosis were assessed.
resultsAc-EEED-induced changes in the morphology of the actin cytoskeleton by inhibiting polymerization of G-actin and disrupting the formation of stress fibers. Pretreatment with Ac-EEED resulted in endothelial cells becoming less responsive to the mitogenic and pro-adhesive effects of VEGF. Ac-EEED treatment in fibroblasts reduced TGF-β-induced fibrosis as assessed by decreased levels of connective tissue growth factor, cysteine-rich 61, collagen I (COL1A2), and collagen III (COL3A1). CNV lesion size and fibrosis were reduced in a concentration-dependent manner by up to 60%.
conclusionsIn vitro studies showed that Ac-EEED affects a broad range of mechanical properties associated with cytoskeletal actin to reduce growth factor effects. The utilization of Ac-EEED in vivo may offer a novel therapeutic strategy by both suppressed neovessel growth and curtailing fibrosis typically associated with the involutional stage of CNV.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.