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Regulation of dystrophin Dp71 during Müller glial cells edema in mouse retina

Abstract : The breakdown of the internal blood-retinal barrier (iBRB) occurs in many retinal disorders and may cause retinal edema, often responsible for vision loss. The aim of this study was to characterize the impact of iBRB disruption on retinal homeostatic changes in Dp71 dystrophin, AQP4 and Kir4.1 caused by Müller glial cells (MGC) alterations. The protective effect of Dex has been studied in this model. In addition, retinal explants were used to study the formation and resolution of CGM edema without the influence of lens inflammation and the effect of different doses of glucocorticoids (Dex, triamcinolone and fluocinolone) and inhibitors of the arachidonic acid pathway. We observed that partial lens surgery induced iBRB breakdown and molecular changes in MGC, decreased expression of Dp71 and AQP4, and miss localization of Kir4.1. Dex seems to protect the retina by increasing the expression of HSF1. We also observed that although the glucocorticoids studied have different effects on the expression of Dp71, AQP4 and Kir4.1 all three can prevent the formation of MGC edema. Our results suggest that edema formation appears to be regulated by leukotrienes. We have studied the role of isoforms of dystrophin Dp71 in intercellular adhesion processes of PC12 cells. Our results suggest the existence of at least two different mechanisms involved in intercellular adhesion associated with Dp71, one involving Dp71dΔ71 and Cx43.
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Submitted on : Wednesday, March 21, 2018 - 11:49:07 AM
Last modification on : Monday, October 26, 2020 - 10:59:06 AM
Long-term archiving on: : Thursday, September 13, 2018 - 8:29:09 AM


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  • HAL Id : tel-01739690, version 1


Lourdes Montserrat Siqueiros Márquez. Regulation of dystrophin Dp71 during Müller glial cells edema in mouse retina. Sensory Organs. Université Pierre et Marie Curie - Paris VI; Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (Mexico), 2017. English. ⟨NNT : 2017PA066361⟩. ⟨tel-01739690⟩



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