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ABSTRACT
Purpose/Aim of the study: Connective tissue growth factor (CTGF) is a key player in the control of extracellular matrix remodeling, fibrosis, and angiogenesis. It is also involved in the modification of the trabecular meshwork, thus potentially modulating outflow facility and intraocular pressure (IOP). As a consequence, CTGF might be relevant for the development of elevated IOP, a major risk factor in glaucoma-pathogenesis. While comprehensive information on the origins of CTGF in the human eye is not available, the goal of this study is to identify ocular sources of CTGF using morphological methods.
Materials and Methods: Human donor eyes were prepared for immunohistochemical analysis of CTGF, α-smooth muscle-actin (ASMA), and CD31. Confocal laser scanning microscopy was used for documentation.
Results: In the cornea, CTGF-immunoreactivity (CTGF-IR) was detected in the epithelium, mainly in basal layers, stromal keratinocytes, and endothelial cells. Adjacent conjunctiva showed also CTGF-IR in epithelial cells. In the iris, both, the sphincter and dilator muscles displayed CGTF-IR, as did iris and ciliary body vessels, deriving at this location from the vascular endothelium, as detected with CD31, but not from vascular smooth muscle cells, as detected with ASMA. In the ciliary body, CTGF-IR was detected in smooth-muscle cells of the ciliary muscle and further in the non-pigmented epithelium. In the retina, CTGF-IR was detected in the NFL and weakly in the IPL/OPL. In the choroid, the choriocapillaris and blood vessels displayed CTGF-IR. Further, few cells in the optic nerve head and the lamina cribrosa were CTGF-positive.
Conclusion: CTGF was detected in various structures of the human eye. Since CTGF has been also described in aqueous humor, the identified structures might be the sources of CTGF in the aqueous humor. By means of aqueous flow, CTGF is transported into the trabecular meshwork, where it could change outflow facility and therefore affecting IOP homeostasis.
Declaration of interests
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
Funding
The present work was supported by the Research Program of Experimental Ophthalmology and Glaucoma Research and the Lotte Schwarz Endowment (Paracelsus Medical University/SALK), Research Fund of the Paracelsus Medical University [grant number E-13/17/088-KAS], The Fuchs-Foundation Austria, Kronprincessan Margaretas Arbetsnämnd för synskadade, Sweden, and Stiftelsen Synfrämjandets Forskningsfond (SFF) Stockholm, Sweden is most gratefully acknowledged. The current study was greatly promoted by the always helpful support of Mrs Virppi Luoma, Emma Lardner, and Anne Winter-Vernersson, BMA at the Cornea Bank of St Eriks Eye Hospital, Stockholm.