Ocular Phenotype of Relaxin Gene Knockout (Rln^-/-) Mice.

Area of Science:

• Ophthalmology
• Genetics
• Molecular Biology

Background:

• Relaxin (Rln) is a hormone with known roles in tissue remodeling.
• Its specific function in ocular structures and its impact on eye diseases are not fully understood.
• Investigating Rln's role is crucial for understanding ocular development and pathology.

Purpose of the Study:

• To determine if relaxin deficiency impacts ocular structure and function.
• To investigate the expression of relaxin and its receptors (Rxfp1, Rxfp2) in ocular tissues.
• To compare ocular phenotypes between relaxin gene knockout (Rln-/-) and wild-type (Rln+/+) mice.

Main Methods:

• RT-PCR and real-time PCR were used to detect Rln, Rxfp1, and Rxfp2 mRNA expression in ocular tissues.
• Ocular phenotypes were assessed in Rln-/- and Rln+/+ mice using optical coherence tomography and rebound tonometry.
• Histological and immunofluorescence analyses were performed on retinal, choroidal, and scleral tissues.

Main Results:

• Rln mRNA was found in the retina, Rxfp1 in the retina, cornea, and sclera/choroid, and Rxfp2 in the cornea.
• Rln-/- mice exhibited higher intraocular pressure, significantly thicker central corneas, larger endothelial cells, and lower endothelial cell density compared to Rln+/+ mice.
• Gene expression analysis revealed significant alterations in corneal and uveal tissues of Rln-/- mice, affecting genes involved in extracellular matrix and fluid transport.

Conclusions:

• Loss of relaxin significantly affects ocular gene expression in the cornea and uvea.
• Relaxin deficiency results in corneal structural changes, including increased thickness and altered endothelial cell characteristics.
• These findings suggest a role for relaxin in regulating extracellular matrix dynamics and fluid balance within the eye.