Role of Lysophospholipid Growth Factors in the Modulation of Aqueous Humor Outflow Facility

2004 ◽  
Vol 45 (7) ◽  
pp. 2263 ◽  
Author(s):  
Priyatham Sai Mettu ◽  
Pei-Feng Deng ◽  
Uma K. Misra ◽  
Govind Gawdi ◽  
David L. Epstein ◽  
...  
Keyword(s):  
Growth Factors ◽  
Aqueous Humor ◽  
Outflow Facility ◽  
Aqueous Humor Outflow

The role of protein kinase C in modulation of aqueous humor outflow facility

2003 ◽  
Vol 76 (1) ◽  
pp. 39-47 ◽  
Author(s):  
Rahul N Khurana ◽  
Pei-Feng Deng ◽  
David L Epstein ◽  
P Vasantha Rao
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Aqueous Humor ◽  
Outflow Facility ◽  
Aqueous Humor Outflow ◽  
Kinase C

5-Methylurapidil, 8-Iso Prostaglandin E2: New Drugs to Increase Aqueous-Humor Outflow Facility

2000 ◽  
pp. 253-259
Author(s):  
J. B. Serle ◽  
S. M. Podos ◽  
R.-F. Wang ◽  
T. Mittag ◽  
P.-Y. Lee ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Aqueous Humor ◽  
New Drugs ◽  
Outflow Facility ◽  
Aqueous Humor Outflow

Role of tissue growth factors in aqueous humor homeostasis

2001 ◽  
Vol 12 (2) ◽  
pp. 94-99 ◽  
Author(s):  
Ulrich Welge-Lüßen ◽  
C. Albrecht May ◽  
Aljoscha S. Neubauer ◽  
Siegfried Priglinger
Keyword(s):  
Growth Factors ◽  
Aqueous Humor ◽  
Tissue Growth

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

PLoS ONE ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. e0161332 ◽  
Author(s):  
Tomokazu Fujimoto ◽  
Toshihiro Inoue ◽  
Kei Maki ◽  
Miyuki Inoue-Mochita ◽  
Hidenobu Tanihara
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Aqueous Humor ◽  
Vascular Endothelial ◽  
Outflow Facility ◽  
Aqueous Humor Outflow ◽  
Endothelial Growth Factor

scholarly journals Effects of Y27632 on Aqueous Humor Outflow Facility With Changes in Hydrodynamic Pattern and Morphology in Human Eyes

2013 ◽  
Vol 54 (8) ◽  
pp. 5859 ◽  
Author(s):  
Chen-Yuan Charlie Yang ◽  
Ye Liu ◽  
Zhaozeng Lu ◽  
Ruiyi Ren ◽  
Haiyan Gong
Keyword(s):  
Aqueous Humor ◽  
Outflow Facility ◽  
Aqueous Humor Outflow ◽  
Human Eyes

scholarly journals Effects of Hydrogen Sulfide-Releasing Compounds on Aqueous Humor Outflow Facility in Porcine Ocular Anterior Segments, Ex Vivo

2017 ◽  
Vol 33 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Jenaye Robinson ◽  
Esther Okoro ◽  
Chinoso Ezuedu ◽  
Leah Bush ◽  
Catherine A. Opere ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Aqueous Humor ◽  
Ex Vivo ◽  
Outflow Facility ◽  
Aqueous Humor Outflow ◽  
Anterior Segments

scholarly journals The role of calcium-independent phospholipase A2γ in modulation of aqueous humor drainage and Ca2+ sensitization of trabecular meshwork contraction

2012 ◽  
Vol 302 (7) ◽  
pp. C979-C991 ◽  
Author(s):  
Padmanabhan P. Pattabiraman ◽  
Fred B. Lih ◽  
Kenneth B. Tomer ◽  
Ponugoti Vasantha Rao
Keyword(s):  
Arachidonic Acid ◽  
Aqueous Humor ◽  
Trabecular Meshwork ◽  
Rho Gtpase ◽  
Focal Adhesions ◽  
Intense Staining ◽  
Outflow Facility ◽  
Bromoenol Lactone ◽  
Mlc Phosphorylation

The contractile and relaxation characteristics of trabecular meshwork (TM) are presumed to influence aqueous humor (AH) drainage and intraocular pressure. The mechanisms underlying regulation of TM cell contractile properties, however, are not well understood. This study investigates the role of calcium-independent phospholipase A2 (iPLA2), which controls eicosanoid synthesis, in regulation of TM cell contraction and AH outflow using mechanism-based isoform specific inhibitors (R)-bromoenol lactone (R-BEL, iPLA2γ specific) and (S)-bromoenol lactone (S-BEL, iPLA2β specific). Immunohistochemical analysis revealed intense staining for both iPLA2β and γ isoforms throughout the TM, juxtacanalicular tissue, and Schlemm's canal of human eye. Inhibition of iPLA2γ by R-BEL or small interfering RNA-mediated silencing of iPLA2γ expression induced dramatic changes in TM cell morphology, and decreased actin stress fibers, focal adhesions, and myosin light-chain (MLC) phosphorylation. AH outflow facility increased progressively and significantly in enucleated porcine eyes perfused with R-BEL. This response was associated with a significant decrease in TM tissue MLC phosphorylation and alterations in the morphology of aqueous plexi in R-BEL-perfused eyes. In contrast, S-BEL did not affect either of these parameters. Additionally, R-BEL-induced cellular relaxation of the TM was associated with a significant decrease in the levels of active Rho GTPase, phospho-MLC phosphatase, phospho-CPI-17, and arachidonic acid. Taken together, these observations demonstrate that iPLA2γ plays a significant and isoform-specific role in regulation of AH outflow facility by altering the contractile characteristics of the TM. The effects of iPLA2γ on TM contractile status appear to involve arachidonic acid and Rho GTPase signaling pathways.

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