Open Access

ARTICLE

Specific Expression of E--Tmod (Tmod1) in Horizontal Cells: Implications in Neuronal Cell Mechanics and Glaucomatous Retina

Weijuan Yao^*, Lanping Amy Sung^†

* Department of Bioengineering, University of California, San Diego La Jolla, CA 92093-0412
† Corresponding author. Department of Bioengineering, And Center for Molecular Genetics, University of California, San Diego. Tel: (858) 534-5250, Email: amysung@bioeng.ucsd.edu

Molecular & Cellular Biomechanics 2009, 6(1), 71-82. https://doi.org/10.3970/mcb.2009.006.071

Abstract

Erythrocyte tropomodulin (E-Tmod) is a tropomyosin-binding and actin capping protein at the point end of the filaments. It is part of a molecular ruler that plays an important role in generating short actin protofilaments critical for the integrity of the cell membrane. Here, with the use of \textit {E-Tmod+/lacZ} mice, we demonstrated a specific E-Tmod expression in horizontal cells (HCs) in the retina, and analyzed the stress-strain relationship of HCs, vertically oriented neurons, and retinal ganglial cells (RGC) under normal and high intraocular pressure (IOP). Since their dendrites are oriented laterally in a plane and form most complicated synapses with multiple cone photoreceptors, HCs are subjected to a greater stress and strain than vertically oriented neurons. The specific E-Tmod expression suggests its role in protecting HCs from mechanical damages in certain eye diseases, such as glaucoma, a neurodegenerative disease of the retina characterized by an elevated IOP. A stress-strain analysis on axons of RGC that run horizontally but only anchor at the optical nerve head suggests that they may also be subjected to a higher mechanical stress, which leads to an increase in ``cup-to-disc'' ratio in a higher IOP or in glaucoma patients.

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