Abstract
As the neural tube forms in the fifth week of human embryonic development, a few ectodermal cells adjacent to the neural plate in the trilaminar embryo, swell, thicken, and compress their intercellular space to form a minute lens placode. At this early stage, the embryonic cells in the lens placode resemble neuroectoderm, enriched in cytoskeletal proteins, junctions, membrane channels, and stress response proteins. With continued differentiation, intracellular organelles disappear to decrease light scattering. The expression of high concentrations of crystallin proteins increase the index of refraction, “n”, for optimal optical function. In each cell, the condensed cytoplasmic proteins organize into the short-range order necessary for maximal transmission of light. Actin, intermediate filaments and microtubules provide a scaffold for the organization of connexins, and aquaporin channels in the membranes supporting a unique microcirculation for the symmetric transport of fluid, ions, and nutrients to the layers of elongating, close-packed, hexagonal cells, the basis for this unique, biological, optical element. The entire optical system is stabilized by molecular and cellular mechanisms designed to protect optical function for a lifetime. Even with the specialized protective mechanisms in lens cells, loss of transparency in cataract formation is one of the most common effects of cellular aging accounting for over 50% of vision impairment worldwide