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Vazquez Membrillo Miguel Angel, Luz Consuelo Zepeda Romero, Francisco Gomez Aguayo, Jose Alfonso Gutierrez Padilla, Eusebio Angulo Castellanos, Juan Carlos Barrera de Leon, Cesareo Gonzalez Bernal, Alejandro Quezada Chalita, Alonso Meza Anguiano, Carmen Clapp; Patients with retinopathy of prematurity (ROP) have increased levels of prolactin and reduced levels of vasoinhibins in the circulation. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5928.
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Prolactin (PRL) is proangiogenic but it acquires antiangiogenic properties after undergoing proteolytic cleavage to vasoinhibins, a family of PRL fragments. Given that preterm infants are hyperprolactinemic and that systemic PRL can access ocular tissues to regulate angiogenesis, we hypothesized that reciprocal changes in the levels of systemic PRL and vasoinhibins contribute to the development and progression of ROP. We therefore compared the levels of PRL and vasoinhibins in the circulation of ROP and control premature infants during the first seven weeks after birth.
Ninety-eight premature patients (birth weight, 500 to 1800 g) matched for gestational age, Apgar score, sepsis, and gender were diagnosed as ROP (n = 53) and control (n = 45) subjects by indirect ophthalmoscopy (at ≥3 weeks postnatal age). PRL was measured by a chemiluminescent immunometric (CI) assay in serum samples obtained every week starting at postnatal week one. Vasoinhibins were evaluated by immunoprecipitation-Western blot and densitometry at postnatal weeks one and three.
Circulating PRL levels were significantly higher in ROP patients than in control patients at week one and at weeks four to seven after birth. These higher levels may reflect the reduced conversion of PRL to vasoinhibins. The CI assay essentially measures PRL, as vasoinhibins have low CI activity (15%). More importantly, the levels of serum vasoinhibins in ROP patients were significantly lower than those in control patients and were undetectable at postnatal weeks one and three, respectively.
These findings show that the ROP condition associates with elevated systemic PRL and its reduced conversion to vasoinhibins. Because PRL and vasoinhibins promote and inhibit angiogenesis, respectively, the reciprocal changes in their levels may represent an efficient mechanism contributing to the development and progression of ROP. Establishing the relation between the levels of PRL and vasoinhibins and infant’s birth weight and severity of ROP will help substantiate these conclusions.
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