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J. Aranda, J. Rivera, H. Quiróz–Mercado, M. Jeziorski, J. Riesgo, G. Nava, G. Martínez de la Escalera, C. Clapp; Endogenous Prolactins Inhibit Angiogenesis in the Retina . Invest. Ophthalmol. Vis. Sci. 2005;46(13):452.
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Purpose: The 16kDa N–terminal fragment of prolactin (16K–PRL) is a potent antiangiogenic factor and may contribute to the inhibition of ocular angiogenesis. 16K–PRL is present in the eye of patients with advanced retinopathy of prematurity, and it can promote apoptosis–mediated vascular regression of newly formed blood vessels (IOVS 45:2049, 2004). Here we investigated the local expression of 16K–PRL in the retina of rats and determined whether it inhibits retinal angiogenesis. Methods: PRL mRNA and proteins in the retina were screened by reverse transcription–polymerase chain reaction, in situ hybridization, and Western blots. The effect of these PRLs on retinal angiogenesis was investigated by the intravitreal injection of anti–PRL antibodies or of small interfering RNAs (siRNA) directed against PRL mRNA. The capillary area was evaluated by the specific staining of retinal blood vessels. Results: PRL mRNA is expressed in rat retinas, and both full–length PRL and 16K–PRL are generated. Anti–PRL antibodies able to neutralize the actions of PRL and 16K–PRL, but not control antibodies or vehicle, increased the retinal capillary area by three–fold. Furthermore, siRNA were able to block local PRL mRNA expression and resulted in significant retinal neovascularization and vasodilatation. Conclusions: PRL and 16K–PRL are synthesized locally in the retina and can exert a tonic inhibition upon retinal angiogenesis and vasodilation.
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