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Prolactin in eyes of patients with retinopathy of prematurity: implications for vascular regression
Zulma Dueñas1, José C Rivera, Hugo Quiróz-Mercado
1Instituto de Neurobiología, Universidad Nacional Autónoma de México, Queretaro, Qro, Mexico.
Insights
The 16K-PRL hormone fragment is found in the eyes of retinopathy of prematurity (ROP) patients and promotes blood vessel regression, contributing to this neovascular eye disease.
Area of Science:
- Ophthalmology
- Endocrinology
- Vascular Biology
Background:
- Neovascular eye diseases like retinopathy of prematurity (ROP) arise from disruptions in the retina's anti-angiogenic environment.
- Prolactin (PRL) is processed into 16K-PRL, a fragment with antiangiogenic and proapoptotic properties.
Purpose of the Study:
- To investigate the presence and role of 16K-PRL in the eyes of ROP patients.
- To determine if 16K-PRL promotes intraocular blood vessel regression in ROP.
Main Methods:
- Quantified PRL in ocular fluids and serum from ROP and control patients.
- Assessed intraocular PRL expression using RT-PCR, in situ hybridization, and Western blot.
- Administered anti-PRL antibodies to neonatal rats to assess hyaloid vessel apoptosis.
Main Results:
- PRL levels were elevated in ROP patients' ocular fluids and serum.
- PRL mRNA and 16 kDa PRL were found in ROP fibrovascular membranes.
- 16K-PRL was more concentrated in subretinal fluid and generated by local proteases.
- Anti-PRL antibodies reduced hyaloid vessel apoptosis in rats.
Conclusions:
- 16K-PRL, whether from circulation or intraocular synthesis, drives apoptosis-induced vascular regression.
- This process contributes to the development and progression of retinopathy of prematurity.
Purpose:
Disruption of the anti-angiogenic environment of the retina leads to neovascular eye diseases, including retinopathy of prematurity (ROP). Prolactin (PRL), the hormone originally associated with milk secretion, is proteolytically processed to 16K-PRL, a fragment with potent antiangiogenic, proapoptotic effects. Whether 16K-PRL is produced in eyes of patients with ROP and promotes the regression of intraocular blood vessels associated with this disease was investigated.
Methods:
PRL was quantified in the aqueous humor, subretinal fluid, and serum from patients with stage 5 ROP and in patients with non-neovascular eye disorders. Intraocular expression of PRL was evaluated by RT-PCR, in situ hybridization, and Western blot analysis. AntiPRL antibodies were injected intravitreously in neonatal rats, and apoptosis of hyaloid vessels determined by TUNEL and ELISA.
Results:
PRL was elevated in ocular fluids and serum from ROP patients. There was no correlation between PRL in ocular fluids and its level in serum, whereas PRL in aqueous humor and subretinal fluid were significantly correlated. PRL mRNA was expressed in blood vessels and leukocytes within retrolental fibrovascular membranes of ROP patients, and these membranes contained a 16 kDa immunoreactive PRL. The 16K-PRL isoform was more concentrated in subretinal fluid than in serum and was generated from PRL by subretinal fluid proteases. Intravitreous injection of neutralizing antiPRL antibodies inhibited the apoptosis of hyaloid vessels in neonatal rats.
Conclusions:
16K-PRL derived from PRL internalized from the circulation or synthesized intraocularly can stimulate apoptosis-induced vascular regression and contribute to the development and progression of ROP.
