Regulation of Lens Morphogenesis and Cataract Pathogenesis by Pituitary-dependent, Insulin-like Mitogens

Abstract

When we started the work to be described, we were not primarily concerned with communication or development in the strictest sense of these terms but with the stimulation of hyperplasia following mechanical wounding of the lens epithelium. Studies from one of our laboratories (Rothstein et al., 1964) as well as those of C.V. Harding, (Harding et al., 1959; Rothstein and Harding, 1962) and N. Rafferty (1963, 1965) showed that mechanical trauma results in the proliferation of lens epithelial cells in teleost, amphibian and mammalian organisms. Unknown to us at the time, similar findings had been reported in the late 19th. century by Th. Leber (1878) and later by Paul Knapp (1900 a, b). In 1882, the immortal Jacob Henle said, “Doch scheint es mir der Mühe werth, auf ein bisher unbeachtetes Organ die Aufmerksamkeit zu lenken, an welchem die Vermehrung der Zellen auf dem Wege der Karyokinese vor sich geht und an welchem sie vielleicht, bei richtiger Wahl des Zeitpunktes, mit grosserer Sicherheit verfolgt werden kann, als an manchen der bisher durchforschten Organe und Gewebe.”. (It certainly seems worth the effort to turn attention to a previously neglected organ, where cell proliferation is achieved by karyokinesis which process could be followed more reliably by an appropriate choice of experimental intervals than in many organs and tissues that have, until now, been exhaustively investigated.) (Figure 1)

“Then there is that little ball of cells which migrated from the skin and thrust itself into the mouth of the eye-stalk.” Sir Charles Sherrington, 1951