June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Vasoinhibins reduce the increase of retinal vasopermeability associated with diabetes: contribution of the kallikrein-kinin system
Author Affiliations & Notes
  • David Arredondo
    Instituto de Neurobiología UNAM, Querétaro, Mexico
  • Olivia Baldivieso Hurtado
    Hospital "Dr. Luis Sanchez Bulnes", Asociación Para Evitar la Ceguera en México, I.A.P., Mexico city, Mexico
  • Daniel Ochoa-Contreras
    Hospital "Dr. Luis Sanchez Bulnes", Asociación Para Evitar la Ceguera en México, I.A.P., Mexico city, Mexico
  • Carmen Clapp
    Instituto de Neurobiología UNAM, Querétaro, Mexico
  • Stephanie Thebault
    Instituto de Neurobiología UNAM, Querétaro, Mexico
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 2696. doi:
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      David Arredondo, Olivia Baldivieso Hurtado, Daniel Ochoa-Contreras, Carmen Clapp, Stephanie Thebault; Vasoinhibins reduce the increase of retinal vasopermeability associated with diabetes: contribution of the kallikrein-kinin system. Invest. Ophthalmol. Vis. Sci. 2013;54(15):2696.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Vasoinhibins are proteolytically-derived fragments of the hormone prolactin that prevent excessive retinal vasopermeability (RVP) associated with diabetes (JCI 118:2291, 2008). The kallikrein-kinin system has been shown to contribute to RVP increase associated with diabetes by enhancing bradykinin (BK) production (Nat Med 13:181, 2007) and inducing B1 receptor expression (PloS One 7:e33864, 2012). Here we investigated if vasoinhibins could attenuate the increase of RVP induced by the intravitreal injection of BK as well as the induction of B1 receptor expression in diabetes.

Methods: The RVP was quantified by the Evans blue method in Wistar male rats that were injected intravitreously with BK (1 nM), combined or not with vasoinhibins (1 µM) or a B2 receptor antagonist (HOE-140). The retinal expression of B1 receptor mRNA was quantified by real-time pcr in two models: 1) healthy rats intravitreously injected with vitreous from patients with proliferative diabetic retinopathy (PDR) for 48 h, and 2) rats rendered diabetic by i.p. streptozotocin for 4 weeks. Both models were also subjected to intra-vitreous injection of vasoinhibins for the last 24 h.

Results: Intravitreal injection of BK resulted in a two-fold increase in RVP compared to saline. Vasoinhibins prevented the BK effect on RVP, as did the B2 receptor antagonist Hoe-140. In addition, mRNA levels of B1 receptor were increased by four- and two-fold in retinas from rats injected with vitreous from PDR patients and diabetic rats compared to rats injected with vitreous from non-diabetic patients and controls, respectively. Notably, vasoinhibins prevented the induction of B1 receptor expression in both models.

Conclusions: Vasoinhibins reduce the BK-induced increase of RVP and the induction of B1 receptor expression related to diabetes.

Keywords: 499 diabetic retinopathy • 715 signal transduction: pharmacology/physiology • 498 diabetes  
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