Vascular Endothelial Growth Factor-A Increases the Aqueous Humor Outflow Facility

Fujimoto, Tomokazu; Inoue, Toshihiro; Maki, Kei; Inoue-Mochita, Miyuki; Tanihara, Hidenobu

doi:10.1371/journal.pone.0161332

Cited by 24 publications

(30 citation statements)

References 26 publications

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“…Proposed mechanisms include obstruction of the conventional outflow pathway by protein aggregates or foreign particles, 17 or damage to the outflow pathway by local inflammation, 15 mechanical trauma, 18 chronic angle closure, 19 or toxicity following repeated injections. 20 Vascular endothelial growth factor may affect outflow facility 21 and we show in our companion study that endogenous VEGF expression in the trabecular meshwork is a paracrine regulator of conventional outflow facility. 22 Although these studies implicate reduced outflow facility as the mechanism for sustained elevated IOP in patients receiving chronic intravitreal anti-VEGF injections, to our knowledge, outflow facility has not been measured in patients receiving prolonged anti-VEGF injections.…”

mentioning

confidence: 75%

Intravitreal Anti-VEGF Injections Reduce Aqueous Outflow Facility in Patients With Neovascular Age-Related Macular Degeneration

Wen

Reina-Torres

Sherwood

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PurposeWe assess the effect of intravitreal anti-VEGF injections on tonographic outflow facility.MethodsPatients with age-related macular degeneration who had received unilateral intravitreal anti-VEGF injections were recruited into two groups, those with ≤10 and those with ≥20 total anti-VEGF injections. Intraocular pressure and tonographic outflow facility of injected and uninjected fellow eyes were measured and compared between groups. Risk factors for development of reduced outflow facility also were assessed.ResultsOutflow facility was 12% lower in the injected eyes of patients who received ≥20 anti-VEGF injections, compared to contralateral uninjected eyes (P = 0.02). In contrast, there was no facility reduction for patients with ≤10 anti-VEGF injections (P = 0.4). In patients with ocular hypertension in the uninjected eye (IOP > 21 mm Hg, n = 5), the outflow facility of injected eyes was on average 46% lower (P = 0.01) than in the uninjected fellow eyes. This was significantly greater than the difference observed in patients with IOP ≤ 21 mm Hg in the uninjected eye (P = 2 × 10−4). In patients with ocular hypertension in the injected eye (n = 6) the differences in facility and IOP between contralateral eyes were significantly greater than in patients with IOP ≤ 21 mm Hg in the injected eye (P = 2 × 10−4 and P = 7 × 10−4, respectively).ConclusionsChronic anti-VEGF injections significantly reduce outflow facility in patients with AMD. The greatest facility reduction is observed in patients with baseline ocular hypertension. Ophthalmologists who administer anti-VEGF injections should be aware of these findings and monitor patients closely for changes in IOP or evidence of glaucoma, especially in those with pre-existing ocular hypertension.

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mentioning

confidence: 75%

Intravitreal Anti-VEGF Injections Reduce Aqueous Outflow Facility in Patients With Neovascular Age-Related Macular Degeneration

Wen

Reina-Torres

Sherwood

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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“…94 Animal studies have demonstrated that VEGF increases aqueous humor outflow facility and that blockage of VEGF receptors leads to ocular hypertension. 35 Anti-VEGF inhibition of the disassembly of the endothelial intercellular junctions, decrease in the endothelial fenestrations, and inhibition of nitric oxide production are a few of the biochemical mechanisms that may explain the impaired outflow and sustained rise in IOP.…”

Section: Long-term Effects Of Intravitreal Anti-vegf Injections mentioning

confidence: 99%

The acute and chronic effects of intravitreal anti-vascular endothelial growth factor injections on intraocular pressure: A review

Bracha

Moore

Ciulla

et al. 2018

Survey of Ophthalmology

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The acute and chronic effects of repeated intravitreal antivascular endothelial growth factor (VEGF) injections on intraocular pressure have not been fully characterized, and the development of sustained ocular hypertension could adversely affect patients who are at risk of glaucomatous optic neuropathy. As expected, volume-driven, acute ocular hypertension immediately follows intravitreal injection, but this pressure elevation is generally transient and well tolerated. Several medications have been investigated to limit acute ocular hypertension following anti-VEGF therapy, but the benefits of pretreatment are not conclusive. Chronic, sustained ocular hypertension, distinct from the short-term acute ocular hypertension after each injection, has also been associated with repeated intravitreal anti-VEGF injections. Risk factors for chronic ocular hypertension include the total number of injections, a greater frequency of injection, and preexisting glaucoma. Proposed mechanisms for chronic ocular hypertension include microparticle obstruction, toxic or inflammatory effects on trabecular meshwork, as well as alterations in outflow facility by anti-VEGF agents. Although limiting anti-VEGF therapy could minimize the risk of both acute and chronic ocular hypertension, foregoing anti-VEGF therapy risks progression of various macular diseases with resulting permanent central vision loss. While definitive evidence of damage to the retinal nerve fiber layer is lacking, patients receiving repeated injections should be monitored for ocular hypertension and patients in whom sustained ocular hypertension subsequently developed should be periodically monitored for glaucomatous changes with optic nerve optical coherence tomography and static visual fields.

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“…At indicated time points (0, 2, 4, 6, 8 hr), the TEER was measured by using Millicell-ERS (Millipore, Germany) as previously described [31][32][33]. The TEER were detected and compared as the percent change from corresponding baseline values.…”

Section: Transendothelial Electrical Resistance (Teer) 2 X 10mentioning

confidence: 99%

Berberine Exerts a Protective Effect on Gut-Vascular Barrier via the Modulation of the Wnt/Beta-Catenin Signaling Pathway During Sepsis

Yuan

Zuo

et al. 2018

Cell Physiol Biochem

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Background/Aims: The gut-vascular barrier (GVB) has recently been depicted to dampen the bacterial invasion of the bloodstream. The intestinal mucosa is a tissue rich in small vessels including capillaries. In this study, the protective effect of berberine on GVB in small bowel mucosa was investigated. Methods: The rat cecal ligation and puncture (CLP) sepsis model was employed to evaluate the effect of berberine on serum endotoxin level and intestinal vascular permeability to Evans blue in vivo. The rat intestinal microvascular endothelial cells (RIMECs) treated by lipopolysaccharide (LPS) were used to assess the effect of berberine on endothelial permeability to FITC-labeled dextran, transendothelial electrical resistance (TEER), and tight junction (TJ) and adherens junction (AJ) expression in vitro. Results: After 24-hr CLP operation the serum endotoxin concentration and gut vascular permeability were significantly increased, while berberine markedly reduced endotoxin level and vascular leakage. In vitro, LPS not only dramatically increased endothelial permeability of RIMECs to FITC-dextran, but also decreased TEER and inhibited claudin-12, beta-catenin and VE-cadherin expression. These effects of LPS were antagonized by berberine. In addition, our in vivo and vitro studies also confirmed that the effect of berberine on GVB could be partially abolished by ICG001. Conclusion: Berberine exerted a protective effect on GVB function in sepsis, which was strictly related to the modulation of the Wnt/beta-catenin signaling pathway.

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Vascular Endothelial Growth Factor-A Increases the Aqueous Humor Outflow Facility

Cited by 24 publications

References 26 publications

Intravitreal Anti-VEGF Injections Reduce Aqueous Outflow Facility in Patients With Neovascular Age-Related Macular Degeneration

Intravitreal Anti-VEGF Injections Reduce Aqueous Outflow Facility in Patients With Neovascular Age-Related Macular Degeneration

The acute and chronic effects of intravitreal anti-vascular endothelial growth factor injections on intraocular pressure: A review

Berberine Exerts a Protective Effect on Gut-Vascular Barrier via the Modulation of the Wnt/Beta-Catenin Signaling Pathway During Sepsis

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