Cellular and Molecular Biology


Repair in avascular tissues: fibrosis in the transparent structures of the eye and thrombospondin 1

P. Hiscott, D. Armstrong, M. Batterbury and S. Kaye

Unit of Ophthalmology, Department of Medicine and Department of Pathology, University of Liverpool, UK

Offprint requests to: Dr. Paul Hiscott, Unit of Ophthalmology, Department of Medicine, University Clinical Departments, Duncan Building, Daulby Street, Liverpool L69 3GA, UK. Fax: + 44 151 706 5802. e-mail: paulsh@liv.ac.uk


Summary. Wound repair is a process which is normally dependent on the vasculature of the damaged tissue. However, the transparent structures of the eye (e.g. central cornea, lens, vitreous) are avascular and yet are still subject to repair and fibrosis. Moreover, the resulting ophthalmic scars often remain avascular. Since this type of ocular scarring may result in blindness, it is the subject of intense research. An aspect of avascular ophthalmic fibrosis which has attracted attention is the question concerning early wound healing components that are usually derived from blood constituents. One such molecule is the glycoprotein thrombospondin 1. Thrombospondin 1 is thought to be a key regulator of cell behaviour in early wound repair and appears to be derived totally from platelet a-granules during repair of incisional skin wounds. It has been shown that the ocular cells involved in avascular repair processes, and which are thus responsible for healing in the absence of platelet-derived thrombospondin 1, are capable of synthesizing the protein themselves. It is suggested that cells involved in ophthalmic repair processes produce thrombospondin 1 in the absence of the platelet-derived molecule. Local synthesis of thrombospondin 1 may represent a therapeutic target in the management of ophthalmic fibrosis. Histol. Histopathol. 14, 1309-1320 (1999)

Key words: Cornea, Lens, Retina, Wound healing, Thrombospondin

DOI: 10.14670/HH-14.1309