Seminar | October 28 | 11:10 a.m.-12:30 p.m. | 489 Minor Hall
David Krizaj, School of Medicine, University of Utah
The vertebrate eye is a biomechanically privileged environment in which intrinsically generated pressure modulates the development, organization and function of ocular tissues. Historically, molecular mechanisms that sense and transduce pressure in the eye tended to be overlooked despite the critical roles their dysregulation might play in visual dysfunctions such as myopia, papilledema and glaucoma. My presentation includes two parts: First, we will discuss the role of mechanotransduction in the regulation of intraocular pressure, with a focus on mechanosensitive TRPV4, piezo and TREK-1 ion channels, focal adhesion proteins and the extracellular matrix within the anterior eye. The second part examines pressure sensing mechanisms in ganglion cells and glia, and their roles in maintaining the mechanical homeostasis. Ion fluxes through mechanoactivated channels regulate neuronal excitability and glial quiescence in the healthy retina, and I will present evidence that their excessive activation contributes to pressure-induced neurodegeneration and inflammation in animal models of glaucoma. The overall suggestion is that dynamic sensing and regulation of biomechanical information is integrated into visual output as an essential component of the multimodal sensory ecosystem within the eye.