Expression, distribution and function of kinin B1 receptor in the rat diabetic retina

Expression, distribution and function of kinin B1 receptor in the rat diabetic retina AbbreviationsBKbradykininDRdiabetic retinopathyGCLganglion cell layerGFAPglial fibrillary acid proteinIba‐1ionized calcium‐binding adapter molecule 1INLinner nuclear layerIPLinner plexiform layerONLouter nuclear layerqRT‐PCRreal‐time quantitative RT‐PCRR‐838Sar‐[D‐Phe8]‐ desArg9‐BKR‐954AcOrn [Oic2, (αMe) Phe5, DβNal7, Ile8] desArg9‐BKRECA‐1rat endothelial cell antigen‐1STZstreptozotocinIntroductionDiabetic retinopathy (DR) is one of the most frequent complications of diabetes. Approximately 75% of patients living with diabetes for 20 years show clinical signs of retinopathy and over 10% of them are affected by a vision loss (Frank, ; Hernandez et al., ). Vision loss is the result of slow and gradual alterations in the microvasculature of the retina due to hyperglycaemia and an inflammatory response, which lead to the overexpression of VEGF, breakdown of the blood‐retinal barrier, pathological proliferation of blood vessels and the formation of fibrous tissue in the vitreous cavity leading to retinal detachment (Wilkinson‐Berka, ). In addition to changes in the vascular bed, pathological mechanisms in DR are associated with activation of glial cells and dysfunction of neurons. Principally, reactive microglia, astrocytes and Müller glial cells in the retina produce VEGF (Wang et al., ; ) and inflammatory mediators that amplify the inflammatory response (Chang et al., ; Sorrentino et al., ) and could play an important role in the breakdown of the haematoretinal barrier (Antonetti et http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png British Journal of Pharmacology Wiley

Expression, distribution and function of kinin B1 receptor in the rat diabetic retina

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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
© 2018 The British Pharmacological Society
ISSN
0007-1188
eISSN
1476-5381
D.O.I.
10.1111/bph.14138
Publisher site
See Article on Publisher Site

Abstract

AbbreviationsBKbradykininDRdiabetic retinopathyGCLganglion cell layerGFAPglial fibrillary acid proteinIba‐1ionized calcium‐binding adapter molecule 1INLinner nuclear layerIPLinner plexiform layerONLouter nuclear layerqRT‐PCRreal‐time quantitative RT‐PCRR‐838Sar‐[D‐Phe8]‐ desArg9‐BKR‐954AcOrn [Oic2, (αMe) Phe5, DβNal7, Ile8] desArg9‐BKRECA‐1rat endothelial cell antigen‐1STZstreptozotocinIntroductionDiabetic retinopathy (DR) is one of the most frequent complications of diabetes. Approximately 75% of patients living with diabetes for 20 years show clinical signs of retinopathy and over 10% of them are affected by a vision loss (Frank, ; Hernandez et al., ). Vision loss is the result of slow and gradual alterations in the microvasculature of the retina due to hyperglycaemia and an inflammatory response, which lead to the overexpression of VEGF, breakdown of the blood‐retinal barrier, pathological proliferation of blood vessels and the formation of fibrous tissue in the vitreous cavity leading to retinal detachment (Wilkinson‐Berka, ). In addition to changes in the vascular bed, pathological mechanisms in DR are associated with activation of glial cells and dysfunction of neurons. Principally, reactive microglia, astrocytes and Müller glial cells in the retina produce VEGF (Wang et al., ; ) and inflammatory mediators that amplify the inflammatory response (Chang et al., ; Sorrentino et al., ) and could play an important role in the breakdown of the haematoretinal barrier (Antonetti et

Journal

British Journal of PharmacologyWiley

Published: Jan 1, 2018

References

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