Person: Yu, Binglan
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Yu
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Binglan
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Yu, Binglan
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Publication The Ability of Nitric Oxide to Lower Intraocular Pressure Is Dependent on Guanylyl Cyclase(The Association for Research in Vision and Ophthalmology, 2017) Muenster, Stefan; Lieb, Wolfgang S.; Fabry, Gregor; Allen, Kaitlin N.; Kamat, Shivani S.; Guy, Ann H.; Dordea, Ana C.; Teixeira, Leandro; Tainsh, Robert E.; Yu, Binglan; Zhu, Wei; Ashpole, Nicole E.; Malhotra, Rajeev; Brouckaert, Peter; Bloch, Donald; Scherrer-Crosbie, Marielle; Stamer, W. Daniel; Kuehn, Markus H.; Pasquale, Louis; Buys, EmmanuelPurpose While nitric oxide (NO) donors are emerging as treatments for glaucoma, the mechanism by which NO lowers intraocular pressure (IOP) is unclear. NO activates the enzyme guanylyl cyclase (GC) to produce cyclic guanosine monophosphate. We studied the ocular effects of inhaled and topically applied NO gas in mice and lambs, respectively. Methods: IOP and aqueous humor (AqH) outflow were measured in WT and GC-1α subunit null (GC-1−/−) mice. Mice breathed 40 parts per million (ppm) NO in O2 or control gas (N2/O2). We also studied the effect of ocular NO gas exposure (80, 250, 500, and 1000 ppm) on IOP in anesthetized lambs. NO metabolites were measured in AqH and plasma. Results: In awake WT mice, breathing NO for 40 minutes lowered IOP from 14.4 ± 1.9 mm Hg to 10.9 ± 1.0 mm Hg (n = 11, P < 0.001). Comparable results were obtained in anesthetized WT mice (n = 10, P < 0.001). In awake or anesthetized GC-1−/− mice, IOP did not change under similar experimental conditions (P ≥ 0.08, n = 20). Breathing NO increased in vivo outflow facility in WT but not GC-1−/− mice (+13.7 ± 14.6% vs. −12.1 ± 9.4%, n = 4 each, P < 0.05). In lambs, ocular exposure to NO lowered IOP in a dose-dependent manner (−0.43 mm Hg/ppm NO; n = 5 with 40 total measurements; P = 0.04) without producing corneal pathology or altering pulmonary and systemic hemodynamics. After ocular NO exposure, NO metabolites were increased in AqH (n = 8, P < 0.001) but not in plasma. Conclusions: Breathing NO reduced IOP and increased outflow facility in a GC-dependent manner in mice. Exposure of ovine eyes to NO lowers IOP.Publication Soluble Guanylate Cyclase a1–Deficient Mice: a novel murine model for Primary Open Angle Glaucoma(Indian Academy of Neurosciences, 2013) Buys, Emmanuel; Ko, Yu-Chieh; Alt, Clemens; Hayton, Sarah R.; Jones, Alexander; Tainsh, Laurel T.; Ren, Ruiyi; Giani, Andrea; Clerte’, Maeva; Abernathy, Emma; Tainsh, Robert E. T.; Oh, Dong-Jin; Malhotra, Rajeev; Arora, Pankaj; de Waard, Nadine; Yu, Binglan; Turcotte, Raphael; Nathan, Daniel; Scherrer-Crosbie, Marielle; Loomis, Stephanie J.; Kang, Jae Hee; Lin, Charles; Gong, Haiyan; Rhee, Douglas J.; Brouckaert, Peter; Wiggs, Janey; Gregory-Ksander, Meredith; Pasquale, Louis; Bloch, Kenneth D.; Ksander, BrucePublication Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation(MyJove Corporation, 2016) O'Rourke, Caitlin; Shelton, Georgia; Hutcheson, Joshua; Burke, Megan F.; Martyn, Trejeeve; Thayer, Timothy E.; Shakartzi, Hannah R.; Buswell, Mary D.; Tainsh, Robert; Yu, Binglan; Bagchi, Aranya; Rhee, David Kwan; Wu, Connie; Derwall, Matthias; Buys, Emmanuel; Yu, Paul; Bloch, Kenneth; Aikawa, Elena; Bloch, Donald; Malhotra, RajeevCardiovascular disease is the leading cause of morbidity and mortality in the world. Atherosclerotic plaques, consisting of lipid-laden macrophages and calcification, develop in the coronary arteries, aortic valve, aorta, and peripheral conduit arteries and are the hallmark of cardiovascular disease. In humans, imaging with computed tomography allows for the quantification of vascular calcification; the presence of vascular calcification is a strong predictor of future cardiovascular events. Development of novel therapies in cardiovascular disease relies critically on improving our understanding of the underlying molecular mechanisms of atherosclerosis. Advancing our knowledge of atherosclerotic mechanisms relies on murine and cell-based models. Here, a method for imaging aortic calcification and macrophage infiltration using two spectrally distinct near-infrared fluorescent imaging probes is detailed. Near-infrared fluorescent imaging allows for the ex vivo quantification of calcification and macrophage accumulation in the entire aorta and can be used to further our understanding of the mechanistic relationship between inflammation and calcification in atherosclerosis. Additionally, a method for isolating and culturing animal aortic vascular smooth muscle cells and a protocol for inducing calcification in cultured smooth muscle cells from either murine aortas or from human coronary arteries is described. This in vitro method of modeling vascular calcification can be used to identify an characterize the signaling pathways likely important for the development of vascular disease, in the hopes of discovering novel targets for therapy.Publication Soluble Guanylate Cyclase α1–Deficient Mice: A Novel Murine Model for Primary Open Angle Glaucoma(Public Library of Science, 2013) Ko, Yu-Chieh; Hayton, Sarah R.; Jones, Alexander; Tainsh, Laurel T.; Ren, Ruiyi; Giani, Andrea; Clerté, Maeva; Abernathy, Emma; de Waard, Nadine; Turcotte, Raphael; Nathan, Daniel; Loomis, Stephanie J.; Gong, Haiyan; Brouckaert, Peter; Buys, Emmanuel; Alt, Clemens; Tainsh, Robert; Oh, Dong-Jin; Malhotra, Rajeev; Arora, Pankaj; Yu, Binglan; Scherrer-Crosbie, Marielle; Kang, Jae Hee; Lin, Charles; Rhee, Douglas J; Wiggs, Janey; Gregory-Ksander, Meredith; Pasquale, Louis; Bloch, Kenneth; Ksander, BrucePrimary open angle glaucoma (POAG) is a leading cause of blindness worldwide. The molecular signaling involved in the pathogenesis of POAG remains unknown. Here, we report that mice lacking the \(α_1\) subunit of the nitric oxide receptor soluble guanylate cyclase represent a novel and translatable animal model of POAG, characterized by thinning of the retinal nerve fiber layer and loss of optic nerve axons in the context of an open iridocorneal angle. The optic neuropathy associated with soluble guanylate cyclase \(α_1\)–deficiency was accompanied by modestly increased intraocular pressure and retinal vascular dysfunction. Moreover, data from a candidate gene association study suggests that a variant in the locus containing the genes encoding for the \(α_1\) and \(β_1\) subunits of soluble guanylate cyclase is associated with POAG in patients presenting with initial paracentral vision loss, a disease subtype thought to be associated with vascular dysregulation. These findings provide new insights into the pathogenesis and genetics of POAG and suggest new therapeutic strategies for POAG.