title: Smad-independent TGF-β2 signaling pathways in human trabecular meshwork cells.
abstract: Aberrant expression and signaling of Transforming Growth Factor (TGF)-β is strongly associated with development of elevated intraocular pressure (IOP) and primary open-angle glaucoma (POAG). In cells of the trabecular meshwork, a key component of the conventional outflow pathway, TGF-β is well-known to promote expression of multiple ocular hypertensive mediators, including genes associated with fibrosis as well as cellular contractility. These effects are mediated by induction of canonical (Smad) as well as non-canonical (MAPK, Rho GTPase) signaling cascades. In the present review, we will highlight the non-canonical, Smad-independent signaling pathways activated by TGF-β2 in human TM cells, as well as the genes known to be induced by non-canonical TGF-β2 signaling.
authors.affiliation: Research Service (151), Department of Veterans Affairs, Edward Hines Jr. VA Hospital, Hines, IL, 60141, USA; Department of Ophthalmology, Loyola University Chicago, Maywood, IL, USA. Electronic address: cynthia.pervan@va.gov.
authors.forename: Cynthia L
authors.initials: CL
authors.lastname: Pervan
mesh_terms: D000818:Animals; D006801:Humans; D020935:MAP Kinase Signaling System / Q000502:physiology; D010766:Phosphorylation; D015398:Signal Transduction / Q000502:physiology*; D051785:Smad Proteins / Q000378:metabolism*; D014129:Trabecular Meshwork / Q000378:metabolism*; D053781:Transforming Growth Factor beta2 / Q000378:metabolism*
chemical_list: D051785:Smad Proteins; D053781:Transforming Growth Factor beta2
keywords: Glaucoma; Intraocular pressure; MAP kinase; Rho GTPase; TGF-β2; Trabecular meshwork