Gene Expression Changes in Steroid-Induced IOP Elevation in Bovine Trabecular Meshwork

Abstract

Steroid-induced IOP elevation alters gene expression in the bovine TM. Identification of genes with changing expression in this model of open-angle glaucoma may help elucidate the primary changes occurring at the molecular level in this condition.

Differential Gene Expression in Glaucoma

“…Microarray studies of gene expression have been conducted using isolated trabecular meshwork cells, organ cultures, and fresh tissue from a variety of animal models and humans (Gonzalez et al 2000;Ishibashi et al 2002;Lo et al 2003;Vittitow and Borras 2004;Zhao et al 2004;Diskin et al 2006;Liton et al 2006;Rozsa et al 2006;Fan et al 2008;Wang et al 2008a;Danias et al 2011;Liu et al 2013). The conditions assayed in these studies were primaryopen angle glaucoma, elevated pressure, and treatment of trabecular meshwork cells with steroids or TGFb.…”

Gene Expression Profile in Human Trabecular Meshwork From Patients With Primary Open-Angle Glaucoma

“…26,27 A number of studies [28][29][30][31][32][33][34][35][36][37][38][39][40][41] have examined gene expression profiles in TM tissue or cells and provided critical information about POAG. However, it remains unclear how the expression profile is affected in TM Copyright 2013 The Association for Research in Vision and Ophthalmology, Inc. www.iovs.org j ISSN: 1552-5783 tissue from patients with POAG compared with that from healthy control subjects.…”

A Porcine Ex Vivo Model of Pigmentary Glaucoma

“…According to the pathway modeling, RhoA signaling, the central pathway that regulates the actin cytoskeleton of the TM, is initiated by exposure to pigment via a complex consisting of insulin growth factor (IGF), the type 1 insulin-like growth factor receptor (IGF-IR), and the lysophosphatidic acid receptor (LPAR) in the cell membrane. This is different from the RhoA activation induced by transforming growth factor (TGF)-β and its receptor in primary open-angle glaucoma 69 and steroid glaucoma 70 . In addition to the inhibition of tight junctions by RhoA, upregulation of the rhophilin Rho GTPase binding protein would also promote reorganizing the TM actin cytoskeleton.…”

“…A change in TM motility could also result from upregulation of a set of chemokine ligands (CCL21/CCL24 and CXCL12/CXCL13) in the cell membrane and Wiskott-Aldrich syndrome protein in the cytoplasm. Activation of the RhoA pathway is seen in primary open-angle glaucoma 69 and in steroid-induced glaucoma 70 . In contrast, with TGF-β-mediated RhoA activation in primary open-angle glaucoma 69 and steroid-induced glaucoma 70 , this process seems initiated by IGF1.…”

“…Activation of the RhoA pathway is seen in primary open-angle glaucoma 69 and in steroid-induced glaucoma 70 . In contrast, with TGF-β-mediated RhoA activation in primary open-angle glaucoma 69 and steroid-induced glaucoma 70 , this process seems initiated by IGF1. IGF1 has been implicated in ocular neovascularisation, 71 and it is tempting to speculate about a role in the uveitis-hyphema-glaucoma syndrome 72 .…”