- •Series Editors
- •Contributors
- •Preface
- •Previous Volumes in Series
- •Relationship of Solute and Water Secretion
- •Centrality of NaCl Secretion
- •Transcellular and Paracellular Components of Secretion
- •Uptake of Stromal NaCl
- •Passage of NaCl from PE to NPE Cells Through Gap Junctions
- •Extrusion of NaCl from NPE Cells to Aqueous Humor
- •Transfer of Water from Stroma to Aqueous Humor
- •Potential Unidirectional Reabsorption of Aqueous Humor
- •Transport Components Underlying Potential Transcellular Reabsorption Across the Ciliary Epithelium
- •References
- •References
- •The Role of Gap Junction Channels in the Ciliary Body Secretory Epithelium
- •Overview
- •General Properties of Connexins Including those Composing the Ciliary Body Epithelium Gap Junctions
- •Animal Models Support a Role for Gap Junctions in Fluid Transport by Ocular Epithelia
- •References
- •Relationship of the EMPA Findings to the Consensus Model for Aqueous Humor Secretion
- •References
- •Functional Modulators Linking Inflow with Outflow of Aqueous Humor
- •Overview
- •Sources of Neuropeptides and Peptide Hormones in the AqH
- •Expression in the Human CB of Glutamate Transporters of the Excitatory Amino Acid Transporters Family
- •Potential Neuroendocrine Entrainment of Circadian Rhythms: AqH Secretion and IOP
- •References
- •Aqueous Humor Outflow Resistance
- •References
- •Aqueous Humor Dynamics I
- •Measurement Methods and Animal Studies
- •Overview
- •Components of Aqueous Humor Dynamics and Measurement Techniques
- •Tonometry
- •Manometry
- •Telemetry
- •Fluorophotometry
- •Confocal Microscopy
- •Aqueous Humor Sampling Method
- •Tonography
- •Fluorophotometry
- •Perfusion Methods
- •Mathematical Calculation
- •Intracameral Tracer Methods
- •Episcleral Venomanometry
- •Direct Cannulation
- •Intracameral Microneedle Method
- •Acknowledgment
- •References
- •Aqueous Humor Dynamics II
- •Dopaminergic Agonists and Antagonists
- •Regulators of the Actin Cytoskeleton
- •Serotonin Agonists
- •References
- •Effects of Circulatory Events on Aqueous Humor Inflow and Intraocular Pressure
- •References
- •Overview
- •Nitric Oxide
- •Glutamate
- •Purines
- •References
- •What is Functional Genomics Teaching us about Intraocular Pressure Regulation and Glaucoma?
- •Functional Genomics: Microarrays, Proteomics and Protein Modification
- •The Trabecular Meshwork Tissue: Expressed Genes (CDNA) and Proteins Obtained by Direct Sequencing and Mass Spectrometry
- •References
- •Molecular Approaches to Glaucoma: Intriguing Clues for Pathology
- •References
- •Outflow Signaling Mechanisms and New Therapeutic Strategies for the Control of Intraocular Pressure
- •Trabecular Pathway
- •Uveoscleral Pathway
- •Carbonic Anhydrase Inhibitors
- •Cholinergics
- •Epinephrine and Analogs
- •Prostaglandin Analogs
- •Cytochalasins
- •Latrunculins
- •Swinholide A
- •Ethacrynic Acid
- •Protein Kinase Inhibitors
- •Broad Spectrum Kinase Inhibitors
- •ROCK Inhibitors
- •CTGF
- •Cochlin
- •References
- •Index
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typically bracketed by gly his and trp asp (GH WD), which may facilitate formation of heterotrimeric or multiprotein complexes. Family members are involved in a variety of cellular processes, such as proliferation, signal transduction, apoptosis, and gene regulation. Two mRNA transcripts for WDR36 were observed at 5.9 and 2.5 kb, which were preferentially expressed in heart, placenta, liver and smooth muscle (Monemi et al., 2005). By RT PCR, expression was found in basically all ocular tissues (Monemi et al., 2005). WDR36 was identified as one of the genes that are upregulated upon T cell activation and was highly co regulated with interleukin 2 (Mao et al., 2004). A specific function is unknown, but may be related to the biogenesis of ribosomal RNA (rRNA), as its homologue in yeast, Utp21, is a protein of the small subunit (SSU) processome which is a large ribonucleoprotein required for the biogenesis of 18S rRNA and with putative roles in both pre rRNA processing and ribosome assembly (Bernstein et al., 2004).
IX. CONCLUSION
As of today, several molecules have been identified that appear to be involved in the pathogenetic processes of POAG. Since an increase in fibrillar ECM in the JCT of the TM is the most characteristic pathological finding in patients with POAG, many of these molecules are involved in the control mechanisms of ECM turnover in the TM outflow pathways. Other molecules have been identified from genetic studies applying linkage analysis and positional cloning. Studies that lead to more complete understanding of these molecules should provide the key to clarify the molecular mechanisms that govern aqueous humor outflow through the TM and the pathogenetic mechanisms of POAG.
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