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Abstract #69384 Published in IGR 18-1

Smad-independent TGF-β2 signaling pathways in human trabecular meshwork cells

Pervan CL
Experimental Eye Research 2017; 158: 137-145


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.

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Classification:

2.5.1 Trabecular meshwork (Part of: 2 Anatomical structures in glaucoma > 2.5 Meshwork)
3.6 Cellular biology (Part of: 3 Laboratory methods)
3.4.2 Gene studies (Part of: 3 Laboratory methods > 3.4 Molecular genetics)



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