Abstract
Eph B1/Ephrin B1 signaling has been shown to play a role in inflammation and pain in some targets; however, its upstream regulation is less clear. To investigate whether exchange protein for cAMP1 (Epac1) can regulate EphB1/ephrin B1 in retinal Müller cells, we generated Epac1-Müller cell specific knockout mice. We used protein analyses to show that Epac1 regulates both EphB1/ephrin B1, as well as high mobility group box 1 (HMGB1) and NLR family pyrin domain containing 3 (NLRP3). Overall, these studies demonstrate the loss of Epac1 in retinal Müller cells increased protein levels of EphB1/ephrin B1, as well as HMGB1 and NLRP3. These mice can be used for future studies on these pathways.
Published Version
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