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Your search keyword '"Yue, Beatrice Y.J.T."' showing total 159 results
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159 results on '"Yue, Beatrice Y.J.T."'

7. A novel role for phagocytosis-like uptake in herpes simplex virus entry

Author

Clement, Christian, Tiwari, Vaibhav, Scanlan, Perry M., Valyi-Nagy, Tibor, Yue, Beatrice Y.J.T., and Shukla, Deepak

Subjects
Herpes simplex virus -- Genetic aspects, Phagocytosis -- Analysis, Biological sciences
Abstract

It is becoming increasingly clear that herpesviruses can exploit the endocytic pathway to infect cells, yet several important features of this process remain poorly defined. Using herpes simplex virus-1 (HSV-1) as a model, we demonstrate that endocytosis of the virions mimic many features of phagocytosis. During entry, HSV-1 virions associated with plasma membrane protrusions followed by a phagocytosis-like uptake involving rearrangement of actin cytoskeleton and trafficking of the virions in large phagosome-like vesicles. RhoA GTPase was activated during this process and the mode of entry was cell type-specific. Clathrin-coated vesicles had no detectable role in virion trafficking as Eps15 dominant-negative mutants failed to affect HSV-1 uptake. Binding and fusion of the virion envelope with the phagosomal membrane is likely facilitated by clustering of nectin-1 (or HVEM) in phagosomes, which was observed in infected cells. Collectively, our data suggests a novel mode of uptake by which the virus can infect both professional and non-professional phagocytes.

Published
2006

12. Histopathologic and immunohistochemical studies of keratoglobus

Author

Meghpara, Beeran, Nakamura, Hiroshi, Vemuganti, Geeta K., Murthy, Somasheila I., Sugar, Joel, Yue, Beatrice Y.J.T., and Edward, Deepak P.

Subjects
Corneal diseases -- Diagnosis, Corneal diseases -- Development and progression, Corneal diseases -- Research, Diagnostic immunohistochemistry -- Research, Health
Published
2009

21. sCD44 overexpression increases intraocular pressure and aqueous outflow resistance

Author

Giovingo, Michael, Nolan, Michael, McCarty, Ryan, Pang, Iok-Hou, Clark, Abbot F., Beverley, Rachel M., Schwartz, Steven, Stamer, W. Daniel, Walker, Loyal, Grybauskas, Algis, Skuran, Kevin, Kuprys, Paulius V., Yue, Beatrice Y.J.T., and Knepper, Paul A.

Subjects
Adult, genetic structures, Genetic Vectors, Immunoblotting, Sus scrofa, Enzyme-Linked Immunosorbent Assay, Adenoviridae, Aqueous Humor, Jurkat Cells, Mice, Young Adult, Membrane Microdomains, Anterior Eye Segment, Trabecular Meshwork, Transduction, Genetic, Animals, Humans, Enzyme Inhibitors, Intraocular Pressure, Mice, Inbred BALB C, Middle Aged, Antibodies, Neutralizing, eye diseases, Actins, Perfusion, Hyaluronan Receptors, Solubility, sense organs, Amyloid Precursor Protein Secretases, Research Article
Abstract

Purpose CD44 plays major roles in multiple physiologic processes. The ectodomain concentration of the CD44 receptor, soluble CD44 (sCD44), is significantly increased in the aqueous humor of primary open-angle glaucoma (POAG). The purpose of this study was to determine if adenoviral constructs of CD44 and isolated 32-kDa sCD44 change intraocular pressure (IOP) in vivo and aqueous outflow resistance in vitro. Methods Adenoviral constructs of human standard CD44 (Ad-CD44S), soluble CD44 (Ad-sCD44), and empty viral cDNA were injected into the vitreous of BALB/cJ mice, followed by serial IOP measurements. Overexpression of CD44S and sCD44 was verified in vitro by enzyme-linked immunosorbent assay (ELISA) and western blot analysis. Anterior segments of porcine eyes were perfused with the isolated sCD44. sCD44-treated human trabecular meshwork (TM) cells and microdissected porcine TM were examined by confocal microscopy and Optiprep density gradient with western blot analysis to determine changes in lipid raft components. Results Intravitreous injection of adenoviral constructs with either Ad-CD44S or Ad-sCD44 vectors caused prolonged ocular hypertension in mice. Eight days after vector injection, Ad-CD44S significantly elevated IOP to 28.3±1.2 mmHg (mean±SEM, n=8; p

Published
2013

22. Suppression of transforming growth factor-β effects in rabbit subconjunctival fibroblasts by activin receptor-like kinase 5 inhibitor

Author

Sapitro, Jennifer, Dunmire, Jeffrey J., Scott, Sarah E., Sutariya, Vijay, Geldenhuys, Werner J., Hewit, Michael, Yue, Beatrice Y.J.T., and Nakamura, Hiroshi

Subjects
Models, Molecular, genetic structures, Pyridines, Blotting, Western, Receptor, Transforming Growth Factor-beta Type I, Fluorescent Antibody Technique, Cell Count, Smad2 Protein, Protein Serine-Threonine Kinases, Transforming Growth Factor beta2, Animals, Benzodioxoles, Phosphorylation, Intraocular Pressure, Binding Sites, Connective Tissue Growth Factor, Imidazoles, Glaucoma, Fibroblasts, eye diseases, Actins, Filtering Surgery, Biological Assay, Rabbits, Conjunctiva, Receptors, Transforming Growth Factor beta, Research Article
Abstract

Purpose Transforming growth factor-β (TGF-β) activity has been implicated in subconjunctival scarring in eyes following glaucoma filtration surgery (GFS). The purpose of this study is to determine whether an inhibitor for activin receptor-like kinase (ALK) 5 (also known as TGF-β receptor type I) could suppress TGF-β activity and thereby promote filtering bleb survival after GFS in a rabbit model. Methods An ALK-5 inhibitor, SB-505124, was used. A docking study was performed to investigate the interaction between the inhibitor and the receptor. Immunofluorescence for connective tissue growth factor (CTGF) and α-smooth muscle actin (α-SMA) was performed in cultured rabbit subconjunctival fibroblasts. Immunoblotting for phosphorylated Smad2 (pSmad2), CTGF, and α-SMA was also performed. In an in vivo rabbit GFS model, SB-505124 was delivered in a lactose tablet during surgery. Eyes were examined by slit-lamp and intraocular pressure (IOP) was measured until the time of bleb failure or up to 28 days after surgery. Tissue sections on day 5 after surgery were histologically evaluated after staining with hematoxylin and eosin. The sections were also immunostained for CTGF and α-SMA. In addition, cell outgrowth from dissected subconjunctival tissues placed in a cell culture flask with media was investigated. Results The docking study indicated hydrogen bond interactions between SB-505124 and amino acids His-283 and Ser-280 of ALK-5. Suppression of pSmad2, CTGF, and α-SMA by SB-505124 was observed in cultured fibroblasts. Filtering blebs in the GFS with SB-505124 group were maintained for more than 10 days, and the period of bleb survival was significantly longer than that in controls. IOP levels after surgery seemed to be related to bleb survival. Histologically, subconjunctival cell infiltration and scarring at the surgical site in the GFS with SB-505124 and mitomycin C (MMC) groups were much subsided compared to controls. Suppression of CTGF and α-SMA by SB-505124 was also observed by immunofluorescence. Cell outgrowth from explants dissected from eyes to which SB-505124 was applied during GFS was robust while outgrowth was poor from those treated with MMC. Conclusions The ALK-5 inhibitor SB-505124 was efficacious both in vitro and in vivo in suppressing the TGF-β action. The inhibitor may provide a novel therapy for preventing ocular inflammation and scarring.

Published
2010

25. Effects of Antiglaucoma Medications on Bovine Trabecular Meshwork Cells In Vitro

Author

Kellogg Eye Center, Department of Ophthalmology, University of Michigan, Ann Arbor, MI, U.S.A., Department of Ophthalmology and Visual Sciences, Lions of Illinois Eye Research Institute, University of Illinois at Chicago College of Medicine, Chicago, IL, USA., Kawa, Jean E., Higginbotham, Eve J., Chang, Isabel L., Yue, Beatrice Y.J.T., Kellogg Eye Center, Department of Ophthalmology, University of Michigan, Ann Arbor, MI, U.S.A., Department of Ophthalmology and Visual Sciences, Lions of Illinois Eye Research Institute, University of Illinois at Chicago College of Medicine, Chicago, IL, USA., Kawa, Jean E., Higginbotham, Eve J., Chang, Isabel L., and Yue, Beatrice Y.J.T.

Abstract

Using an in vitro culture system, we investigated the effects of five antiglaucoma drugs on growth and morphologic characteristics of bovine trabecular meshwork cells. Epinephrine hydrochloride (55-550 [mu]M) and pilocarpine hydrochloride (0[middle dot]8-16 mM), when added to the cultures for 3 days, inhibited trabecular cell growth in a dose-dependent manner. The lowest concentration at which the inhibitory effect was observed was 109 [mu]M and 0[middle dot]8 mM, respectively, for epinephrine and pilocarpine. Dipivefrin hydrochloride (26-260 [mu]M), timolol maleate (116-1160 [mu]M), and levobunolol hydrochloride (150-1500 [mu]M) were also added to the cells for 3 days. These drugs caused a reduction in cell density, respectively, at concentrations higher than 103, 460, and 616 [mu]M. Cell elongation was seen in cultures treated with epinephrine and dipivefrin, whereas levobunolol and timolol induced the cells to adopt a rounded appearance. Cells that had been exposed to pilocarpine were enlarged with numerous vacuoles. By scanning electron microscopic techniques, epinephrine, timolol, and levobunolol were found to retard the phagocytosis of latex beads by trabecular meshwork cells. Immunostaining with the use of antibodies to vimentin and actin revealed disorganization and condensation of cytoskeletal fibers in trabecular meshwork cells after treatment with epinephrine and dipivefrin. Little change was seen with comparable concentrations of a preservative, benzalkonium chloride, and a vehicle, Liquifilm tears. These results showed that antiglaucoma drugs, depending on their concentrations, may profoundly influence the growth and activity of trabecular meshwork cells.

Published
2006

49. Interaction between two glaucoma genes, optineurin and myocilin.

Author

Bum-Chan Park, Tibudan, Martin, Samaraweera, Mishan, Xiang Shen, and Yue, Beatrice Y.J.T.

Subjects
GENES, GLAUCOMA, NERVE growth factor, MESSENGER RNA, EYE diseases
Abstract

Myocilin (MYOC) and optineurin (OPTN) are two genes linked to glaucoma, a major blinding disease. To investigate the possible molecular interactions between MYOC and OPTN genes, we over-expressed MYOC and examined its effect on the level of endogenous OPTN in human trabecular meshwork (TM) cells and vice versa. We noted that over-expressing MYOC did not affect the OPTN level, whereas OPTN over-expression induced an up-regulation of the endogenous MYOC. This induction was also observed in other ocular and non-ocular cell types including PC12 cells. The endogenous levels of both OPTN and MYOC genes were in addition found increased when PC12 cells underwent differentiation upon treatment with nerve growth factor (NGF). Over-expression of OPTN resulted in prolonged turnover rate of MYOC mRNA but had little effect on the promoter activity of the MYOC gene. The over-expressed OPTN was localized in the cytoplasm, not translocated into the nucleus. These results indicate that interaction exists between OPTN and MYOC genes. Regulation of MYOC expression by OPTN is achieved primarily through control of the mRNA stability. [ABSTRACT FROM AUTHOR]

Published
2007
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