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Updated: May 7, 2026

Dissection of Human Vitreous Body Elements for Proteomic Analysis
Published on: January 23, 2011
Vitreous Fibrillar Structure and Interfibrillar Composition in Adult Mice
Patricia Jaramillo-Garcés1,2,3, Judit Pampalona4, Ana Carretero1,2,3
1Centre for Animal Biotechnology and Gene Therapy (CBATEG), Universitat Autònoma de Barcelona, Bellaterra, Spain.
Purpose:
Although mice are widely used models for human eye diseases, knowledge of their vitreous is scarce and fragmentary. This study characterizes the structure and composition of vitreous fibrils and their interfibrillar space. Given the role of this fibrillar network in maintaining the vitreous' biomechanical properties, the impact of intravitreal injections on vitreous architecture was also explored.
Methods:
Healthy adult C57/BL6J mice were studied. Classical histological techniques, picrosirius red-polarization, immunofluorescence, lectin histochemistry, and hyaluronic acid binding protein assays were used to examine vitreous fibrils and interfibrillar space. For the analysis of distribution of components along the fibrils, the Airyscan microscopy was used to achieve higher resolution.
Results:
Vitreous fibrils consist of fibrillar collagen, glycoproteins (fibrillin 1, fibronectin, laminin, and collagen IV), N-acetyl galactosamine, and hyaluronan, all absent in the interfibrillar space. A single sterile intravitreal saline injection induced an inflammatory insult, characterized by increased fibril density and macrophage/hyalocyte invasion. Lysosome-associated membrane protein 1 (Lamp1) immunohistochemistry suggests these cells may remove fibrils via phagocytosis and activate a remodeling process in the vitreous.
Conclusions:
This study enhances understanding of the mouse vitreous structure, suggesting fibrils are composed of glycoprotein-wrapped collagen cores. Furthermore, the absence of hyaluronan and glycoproteins between fibrils may explain lower viscosity in mice compared with humans. Intravitreal injections as an inflammatory insult disrupt fibril networks and activate macrophages/hyalocytes.
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