Effects of Genipin Crosslinking of Porcine Perilimbal Sclera on Mechanical Properties and Intraocular Pressure.
crosslinking
fluorescence
genipin
intraocular pressure
perfusion
perilimbal sclera
strain rate
stress relaxation
tangent modulus
viscoelasticity
Journal
Bioengineering (Basel, Switzerland)
ISSN: 2306-5354
Titre abrégé: Bioengineering (Basel)
Pays: Switzerland
ID NLM: 101676056
Informations de publication
Date de publication:
02 Oct 2024
02 Oct 2024
Historique:
received:
09
08
2024
revised:
17
09
2024
accepted:
25
09
2024
medline:
25
10
2024
pubmed:
25
10
2024
entrez:
25
10
2024
Statut:
epublish
Résumé
The mechanical properties of sclera play an important role in ocular functions, protection, and disease. Modulating the sclera's properties by exogenous crosslinking offers a way to expand the tissue's range of properties for study of the possible influences on the eye's behavior and diseases such as glaucoma and myopia. The focus of this work was to evaluate the effects of genipin crosslinking targeting the porcine perilimbal sclera (PLS) since the stiffness of this tissue was previously found in a number of studies to influence the eye's intraocular pressure (IOP). The work includes experiments on tensile test specimens and whole globes. The specimen tests showed decreased strain-rate dependence and increased relaxation stress due to the cross-linker. Whole globe perfusion experiments demonstrated that eyes treated with genipin in the perilimbal region had increased IOPs compared to the control globes. Migration of the cross-linker from the target tissue to other tissues is a confounding factor in whole globe, biomechanical measurements, with crosslinking. A novel quantitative genipin assay of the trabecular meshwork (TM) was developed to exclude globes where the TM was inadvertently crosslinked. The perfusion study, therefore, suggests that elevated stiffness of the PLS can significantly increase IOP apart from effects of the TM in the porcine eye. These results demonstrate the importance of PLS biomechanics in aqueous outflow regulation and support additional investigations into the distal outflow pathways as a key source of outflow resistance.
Identifiants
pubmed: 39451372
pii: bioengineering11100996
doi: 10.3390/bioengineering11100996
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : National Science Foundation
ID : CMMI 1760291
Organisme : NEI NIH HHS
ID : P30EY007003
Pays : United States
Organisme : NIDDK NIH HHS
ID : 1R01DK12568701
Pays : United States