ArticleInvestigative ophthalmology & visual science2009
Identification of the active site in the heparin II domain of fibronectin that increases outflow facility in cultured monkey anterior segments.
Article in Investigative ophthalmology & visual science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Integrin α4 and α9 in trabecular meshwork and Schlemm's canal function: emerging regulators of intraocular pressure homeostasis.Frontiers in cell and developmental biology · 2026Review
- Pathogenesis of glaucoma: Extracellular matrix dysfunction in the trabecular meshwork-A review.Clinical & experimental ophthalmology · 2022Review
- Integrin Crosstalk and Its Effect on the Biological Functions of the Trabecular Meshwork/Schlemm's Canal.Frontiers in cell and developmental biology · 2022Review
- Review
- The role of integrins in glaucoma.Experimental eye research · 2017Review
- Tissue-based multiphoton analysis of actomyosin and structural responses in human trabecular meshwork.Scientific reports · 2016Article
- Mixed Fibronectin-Derived Peptides Conjugated to a Chitosan Matrix Effectively Promotes Biological Activities through Integrins, α4β1, α5β1, αvβ3, and Syndecan.BioResearch open access · 2016Article
- Aqueous humor outflow: dynamics and disease.Investigative ophthalmology & visual science · 2015Review
- Cellular fibronectin expression in human trabecular meshwork and induction by transforming growth factor-β2.Investigative ophthalmology & visual science · 2013Article
- The effects of tenascin C knockdown on trabecular meshwork outflow resistance.Investigative ophthalmology & visual science · 2013Article
- Integrins in trabecular meshwork and optic nerve head: possible association with the pathogenesis of glaucoma.BioMed research international · 2013Review
- Two-photon immunofluorescence characterization of the trabecular meshwork in situ.Investigative ophthalmology & visual science · 2012Article
- Inhibition of hyaluronan synthesis reduces versican and fibronectin levels in trabecular meshwork cells.PloS one · 2012Article
- Integrin-linked kinase regulates integrin signaling in human trabecular meshwork cells.Investigative ophthalmology & visual science · 2011Article
- Heparin II domain of fibronectin mediates contractility through an alpha4beta1 co-signaling pathway.Experimental cell research · 2010Article
- Functional properties of fibronectin in the trabecular meshwork.Experimental eye research · 2009Review
- The role of integrins in the trabecular meshwork.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and TherapeuticsReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo determine the active site in the Heparin II (HepII) domain of fibronectin that regulates outflow facility in cultured anterior segments and disrupts the actin cytoskeleton in transformed human trabecular meshwork (TM-1) cells.
methodsOutflow facility was determined by two-level, constant-pressure perfusion in cultured anterior segments of rhesus and cynomolgus monkey eyes. One segment from each pair was exchanged with either the HepII domain or an integrin/syndecan binding peptide (IDAPS or PPRARI) from the HepII domain. To assay changes in the actin cytoskeleton, TM-1 cells were incubated for 24 hours with or without the HepII domain, PPRARI, or IDAPS. Changes were monitored with phase and immunofluorescence microscopy.
resultsHepII domain (100 microg/mL) and PPRARI (500 microg/mL) increased outflow facility by 31% +/- 13% (n = 9, P < 0.05) and 24% +/- 9% (n = 8, P < 0.05), respectively in cultured anterior segments after an overnight infusion. Perfusion with IDAPS (500 microg/mL) had no effect on outflow facility. In TM-1 cultures, 250 microg/mL of the HepII domain or 4 mg/mL of PPRARI disrupted the assembly of actin filaments. A lower concentration of PPRARI (2 mg/mL) disrupted the actin cytoskeleton when used in combination with a nondisrupting concentration of the HepII domain (30-60 microg/mL). In contrast, IDAPS did not disrupt the actin cytoskeleton under any condition tested.
conclusionsThe active site in the HepII domain that regulates outflow facility in cultured anterior segments and disrupts the actin cytoskeleton in TM-1 cells is the syndecan/integrin binding sequence, PPRARI.
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