title: Extracellular matrix turnover and outflow resistance.
abstract: Normal homeostatic adjustment of elevated intraocular pressure (IOP) involves remodeling the extracellular matrix (ECM) of the trabecular meshwork (TM). This entails sensing elevated IOP, releasing numerous activated proteinases to degrade existing ECM and concurrent biosynthesis of replacement ECM components. To increase or decrease IOP, the quantity, physical properties and/or organization of new components should be somewhat different from those replaced in order to modify outflow resistance. ECM degradation and replacement biosynthesis in the outflow pathway must be tightly controlled and focused to retain the complex structural organization of the tissue. Recently identified podosome- or invadopodia-like structures (PILS) may aid in the focal degradation of ECM and organization of replacement components.
authors.affiliation: Casey Eye Institute, Oregon Health and Science University, Portland, OR 97239-4197, USA.
authors.forename: Kate E
authors.initials: KE
authors.lastname: Keller
authors.forename: Mini
authors.initials: M
authors.lastname: Aga
authors.forename: John M
authors.initials: JM
authors.lastname: Bradley
authors.forename: Mary J
authors.initials: MJ
authors.lastname: Kelley
authors.forename: Ted S
authors.initials: TS
authors.lastname: Acott
mesh_terms: D005109:Extracellular Matrix / Q000378:metabolism*; D016326:Extracellular Matrix Proteins / Q000502:physiology; D006801:Humans; D007429:Intraocular Pressure / Q000502:physiology*; D020782:Matrix Metalloproteinases / Q000502:physiology; D008666:Metalloendopeptidases / Q000502:physiology; D019714:Tissue Inhibitor of Metalloproteinases / Q000502:physiology; D014129:Trabecular Meshwork / Q000502:physiology*
chemical_list: D016326:Extracellular Matrix Proteins; D019714:Tissue Inhibitor of Metalloproteinases; D020782:Matrix Metalloproteinases; D008666:Metalloendopeptidases; C028220:Crotalus adamanteus proteinase II