Development of a rabbit model of persistent hypotony without ciliary body injury.

In order to study the pathophysiological alterations of the ciliary body (CB) during persistent hypotony, it is necessary to develop an animal model without CB injury. In this study, we successfully established a modified model of persistent hypotony without CB injury in New Zealand rabbits. A 23-gauge pars plana vitrectomy (PPV) was performed and a trocar-formed fistula was allowed to remain in situ, to produce a continuous outflow of intraocular fluid.

Molecular Tweezers-like Calix[4]arene Based Alkaline Earth Metal Cation (Ca, Sr, and Ba) Chemosensor and Its Imaging in Living Cells and Zebrafish.

Although alkaline earth metal cations play an important role in our daily life, little attention has been paid to the field of fast quantitative analysis of their content due to a lack of satisfactory precision and a fast and convenient means of detection. In this study, we have designed a set of molecular tweezers based on the calix[4]arene chemosensor , which was found to exhibit high selectivity and sensitivity toward Ca, Sr, and Ba (by UV-vis and fluorescence methods) with low detection limits of the order of 10 to 10 M and high association constants (of the order of 10). More significantly, sensor not only can recognize Ca, Sr, and Ba but also can further discriminate between these three cations via the differing red shifts in their UV-vis spectra (560 nm for ·Ca, 570 nm for ·Sr, and 580 nm for ·Ba complex) which is attributed to their different atomic radii.

Activation of Toll-like receptor 3 promotes pathological corneal neovascularization by enhancement of SDF-1-mediated endothelial progenitor cell recruitment.

Toll-like receptors (TLRs) play an important role in inflammatory and immunological responses, which are intimately related to neovascularization. However, the precise mode of action of TLR3 in neovascularization still remains ambiguous. In this study, we sought to investigate the role of TLR3 in pathological corneal neovascularization (CNV) using a mouse model of alkali-induced CNV.

SIS3, a specific inhibitor of smad3, attenuates bleomycin-induced pulmonary fibrosis in mice.

Pulmonary fibrosis (PF) is a fatal respiratory disease with no effective medical treatments available. TGF-β/Smads signaling has been implicated to play an essential in the pathogenesis of PF, in which Smad3 act as the integrator of pro-fibrosis signals. In this study, we determined the effect of SIS3, a specific inhibitor of Smad3, in an experimental mouse model of lung fibrosis.

Interleukin 37 promotes angiogenesis through TGF-β signaling.

IL-37 is a novel pro-angiogenic cytokine that potently promotes endothelial cell activation and pathological angiogenesis in our previous study, but the mechanisms behind the pro-angiogenic effect of IL-37 are less well understood. Extending our observations, we found that TGF-β interacts with IL-37, and potently enhances the binding affinity of IL-37 to the ALK1 receptor complex, thus allowing IL-37 to signal through ALK1 to activate pro-angiogenic responses. We further show that TGF-β and ALK1 are required in IL-37 induced pro-angiogenic response in ECs and in the mouse model of Matrigel plug and oxygen-induced retinopathy.

The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy.

Interleukin 38 (IL-38) is a novel identified cytokine of IL-1 family in which some members are important in inflammation and angiogenesis. However, the role of IL-38 in regulating angiogenesis is unknown. The aim of the present study is to explore the effect of IL-38 on angiogenesis.

IL-37 impairs host resistance to Listeria infection by suppressing macrophage function.

Listeria monocytogenes is a Gram-positive intracellular bacterium that was transmitted through contaminated food and causes sepsis and even death. IL-37 has been described as an important anti-inflammatory factor, but little is known about the function of IL-37 in host defense against Liseria monocytogenes (Lm) infection. In mice model of systemic infection, we found that mice treated with IL-37 were more sensitive to Lm infection compared with PBS-treated mice.

Involvement of IL-37 in the Pathogenesis of Proliferative Diabetic Retinopathy.

Purpose: Interleukin-37 is suggested as a novel proangiogenic factor in our previous study. In this study, the role of IL-37 was investigated in proliferative diabetic retinopathy (PDR).

Methods: Vitreous fluids from 10 patients with PDR and 8 controls were collected.

T-helper-associated cytokines expression by peripheral blood mononuclear cells in patients with polypoidal choroidal vasculopathy and age-related macular degeneration.

Background: Immune responses play a key role in the pathogenesis and progression of polypoidal choroidal vasculopath (PCV) and age-related macular degeneration (AMD). In this study, we determined the Th cell-associated immune responses by measuring the cytokine expression of peripheral blood mononuclear cells (PBMC) in both PCV and neovascular AMD (nAMD) patients.

Methods: Twenty-seven nAMD patients, 33 PCV patients and a gender- and age-matched group of 18 healthy individuals were involved in this study.

Formylpeptide receptor 1 mediates the tumorigenicity of human hepatocellular carcinoma cells.

G protein-coupled chemoattractant receptors (GPCRs) have been implicated in cancer progression. Formylpeptide receptor 1 (FPR1) was originally identified as a GPCR mediating anti-microbial host defense. However, the role of FPR1 in tumorigenesis remains poorly understood.

Topical Application of Interleukin-28A Attenuates Allergic Conjunctivitis in an Ovalbumin-Induced Mouse Model.

Purpose: Allergic conjunctivitis (AC) is an immunoglobulin E (IgE)-mediated and helper T cell 2 (Th2)--cell-mediated disease characterized by conjunctival eosinophilic infiltration. Previous study shows that IL-28A had anti-allergic activity in airway disease. In this study, we examined the effect of IL-28A on a mouse model of ovalbumin (OVA)-induced experimental allergic conjunctivitis (EAC).

IL-37 Is a Novel Proangiogenic Factor of Developmental and Pathological Angiogenesis.

Objective: Angiogenesis is tightly controlled by growth factors and cytokines in pathophysiological settings. Interleukin 37 (IL-37) is a newly identified cytokine of the IL-1 family, some members of which are important in inflammation and angiogenesis. However, the function of IL-37 in angiogenesis remains unknown.

High glucose induces and activates Toll-like receptor 4 in endothelial cells of diabetic retinopathy.

Background: Hyperglycemia-induced inflammation causes the dysfunction of blood vessels, and Toll-like receptor 4 (TLR4) plays a key role in inflammation-induced angiogenesis. However, the impact of TLR4 on the pathogenesis of diabetic retinopathy (DR) is poorly understood. In this study, we examined the expression of TLR4 in retinal vascular endothelial cells of patients with DR and diabetic mice, and explored the role of TLR4 in mediating inflammatory responses by human microvascular endothelial cells (HMEC-1) under high-glucose condition.

AA092, an annonaceous acetogenin mimetic, attenuates angiogenesis in a mouse model of inflammation-induced corneal neovascularization.

Previous studies demonstrated that annonaceous acetogenin (AA) was an antitumor drug with anti-angiogenic activity. However, the effect of AA on ocular neovascular disorders remains unclear. The aim of the present study is to explore the effect of AA092, an annonaceous acetogenin mimetic, on corneal neovascularization (CNV).

Neuroinflammatory responses in diabetic retinopathy.

Diabetic retinopathy (DR) is a common complication of diabetes and has been recognized as a vascular dysfunction leading to blindness in working-age adults. It becomes increasingly clear that neural cells in retina play an important role in the pathogenesis of DR. Neural retina located at the back of the eye is part of the brain and a representative of the central nervous system.

High-mobility group box-1-Toll-Like receptor 4 axis mediates the recruitment of endothelial progenitor cells in alkali-induced corneal neovascularization.

Endothelial progenitor cells (EPCs) promote both physiological and pathological neovascularization. Recently we found high-mobility group box-1 (HMGB1)-Toll-like receptor 4 (TLR4) signaling pathway promotes corneal neovascularization (CNV) induced by alkali in a mouse model. However, it is still unclear whether HMGB1-TLR4 promotes the mobility of EPCs.

Suberoylanilide hydroxamic acid suppresses inflammation-induced neovascularization.

Histone deacetylases (HDACs) regulate gene transcription by modifying the acetylation of histone and nonhistone proteins. Deregulated expression of HDACs has been implicated in tumorigenesis and angiogenesis. In this study, we examined the effect of suberoylanilide hydroxamic acid (SAHA), a potent inhibitor of HDACs, on inflammatory corneal angiogenesis.

Interleukin-28A enhances autoimmune disease in a retinal autoimmunity model.

Interleukin-28A (IL-28A), a member of type III interferons (IFN-λs), promotes antiviral, antitumor and immune responses. However, its ability to regulate autoimmune diseases is poorly understood. In this study, we examined the effect of IL-28A on retinal antigen-induced experimental autoimmune uveoretinitis (EAU), a mouse model of human T-cell-mediated autoimmune eye disease.

Interleukin-1β promotes the induction of retinal autoimmune disease.

Interleukin-1β (IL-1β) is a potent proinflammatory cytokine that plays a critical role in initiating immunoinflammatory responses. In this study, we generated recombinant mouse IL-1β and anti-mouse IL-1β polyclonal antibodies to examine the effect of IL-1β on experimental autoimmune uveoretinitis (EAU), a mouse model for T cell-mediated eye autoimmune disease. Administration of mouse IL-1β by i.

Largazole, an inhibitor of class I histone deacetylases, attenuates inflammatory corneal neovascularization.

Histone deacetylases (HDACs) regulate gene transcription by modifying the acetylation level of histone and nonhistone proteins. In this study, we examined the effect of largazole, an inhibitor of class I HDACs, on inflammatory corneal angiogenesis. In a mouse model of alkali-induced corneal neovascularization (CNV), topical application of largazole to the injured corneas attenuated CNV.

Interleukin-28A promotes IFN-γ production by peripheral blood mononuclear cells from patients with Behçet's disease.

Behçet's disease (BD) is an autoimmune disease of unknown etiology. Interleukin-28A (IL-28A) promotes immune responses and may participate in the pathogenesis of autoimmune diseases. To examine the role of IL-28A in the pathogenesis of BD, we measured the expression of IFN-γ and IL-17 by IL-28A-stimulated peripheral blood mononuclear cells (PBMCs) from 19 patients with BD and 16 healthy individuals.

A critical role for interleukin-1β in the progression of autoimmune diseases.

Interleukin-1β (IL-1β) belongs to IL-1 family and is a potent pro-inflammatory cytokine. It is known to be also involved in a variety of cellular activities, including cell proliferation, differentiation and apoptosis. In addition to its pathophysiologic role in host protection, IL-1β promotes the progression of a number of autoimmune diseases.

Angiogenesis mediated by toll-like receptor 4 in ischemic neural tissue.

Objective: Activation of the immune system via toll-like receptors (TLRs) is implicated in atherosclerosis, microvascular complications, and angiogenesis. However, the involvement of TLRs in inflammation-associated angiogenesis in ischemic neural tissue has not been investigated. The goal of this study is to determine the role of TLR4 signaling in oxygen-induced neovascularization in retina, a neural tissue.

The expression of Toll-like receptors in murine Müller cells, the glial cells in retina.

Müller cells, the principal glial cells of the retina, play an important role in immune responses. Toll-like receptors (TLRs) are members of the pattern recognition receptor family and mediate innate and adaptive immune responses. In this study, we isolated, characterized Müller cells from mouse retina, and analyzed the expression of TLRs in these cells.

Toll-like receptor 3 ligand polyinosinic:polycytidylic acid promotes wound healing in human and murine skin.

Toll-like receptors (TLRs) are pattern-recognition receptors and have a critical role in both innate and adaptive responses to tissue injury. Our previous study showed that wound healing was impaired in TLR3-deficient mice. In this study, we investigated the capacity of the TLR3 agonist polyriboinosinic-polyribocytidylic acid (poly(I:C)) to promote the healing of skin wounds in humans and mice.