Hyalocytes-guardians of the vitreoretinal interface.

Clemens Lange, Peter Wieghofer, J Sebag, Stefaniya Boneva

Journal: Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie 2024;262(9):2765-2784

PMID: 38568222

Abstract

Originally discovered in the nineteenth century, hyalocytes are the resident macrophage cell population in the vitreous body. Despite this, a comprehensive understanding of their precise function and immunological significance has only recently emerged. In this article, we summarize recent in-depth investigations deciphering the critical role of hyalocytes in various aspects of vitreous physiology, such as the molecular biology and functions of hyalocytes during development, adult homeostasis, and disease. Hyalocytes are involved in fetal vitreous development, hyaloid vasculature regression, surveillance and metabolism of the vitreoretinal interface, synthesis and breakdown of vitreous components, and maintenance of vitreous transparency. While sharing certain resemblances with other myeloid cell populations such as retinal microglia, hyalocytes possess a distinct molecular signature and exhibit a gene expression profile tailored to the specific needs of their host tissue. In addition to inflammatory eye diseases such as uveitis, hyalocytes play important roles in conditions characterized by anomalous posterior vitreous detachment (PVD) and vitreoschisis. These can be hypercellular tractional vitreo-retinopathies, such as macular pucker, proliferative vitreo-retinopathy (PVR), and proliferative diabetic vitreo-retinopathy (PDVR), as well as paucicellular disorders such as vitreo-macular traction syndrome and macular holes. Notably, hyalocytes assume a significant role in the early pathophysiology of these disorders by promoting cell migration and proliferation, as well as subsequent membrane contraction, and vitreoretinal traction. Thus, early intervention targeting hyalocytes could potentially mitigate disease progression and prevent the development of proliferative vitreoretinal disorders altogether, by eliminating the involvement of vitreous and hyalocytes.

© 2024. The Author(s).

Address: Department of Ophthalmology, St. Franziskus Hospital, Muenster, Germany. [email protected].; Eye Center, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany. [email protected].; Eye Center, Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.; Cellular Neuroanatomy, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Augsburg, Germany.; VMR Institute for Vitreous Macula Retina, Huntington Beach, CA, USA. [email protected].; Doheny Eye Institute, UCLA, Pasadena, CA, USA. [email protected].; Department of Ophthalmology, Geffen School of Medicine, UCLA, Los Angeles, CA, USA. [email protected].

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