| First Author | Jiang Y | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 7 | Pages | e70555 |
| PubMed ID | 23894672 | Mgi Jnum | J:204379 |
| Mgi Id | MGI:5532430 | Doi | 10.1371/journal.pone.0070555 |
| Citation | Jiang Y, et al. (2013) beta2-adrenergic receptor knockout mice exhibit A diabetic retinopathy phenotype. PLoS One 8(7):e70555 |
| abstractText | There is considerable evidence from our lab and others for a functional link between beta-adrenergic receptor and insulin receptor signaling pathways in retina. Furthermore, we hypothesize that this link may contribute to lesions similar to diabetic retinopathy in that the loss of adrenergic input observed in diabetic retinopathy may disrupt normal anti-apoptotic insulin signaling, leading to retinal cell death. Our studies included assessment of neural retina function (ERG), vascular degeneration, and Muller glial cells (which express only beta1 and beta2-adrenergic receptor subtypes). In the current study, we produced beta2-adrenergic receptor knockout mice to examine this deletion on retinal neurons and vasculature, and to identify specific pathways through which beta2-adrenergic receptor modulates insulin signaling. As predicted from our hypothesis, beta2-adrenergic receptor knockout mice display certain features similar to diabetic retinopathy. In addition, loss of beta2-adrenergic input resulted in an increase in TNFalpha, a key inhibitor of insulin receptor signaling. Increased TNFalpha may be associated with insulin-dependent production of the anti-apoptotic factor, Akt. Since the effects occurred in vivo under normal glucose conditions, we postulate that aspects of the diabetic retinopathy phenotype might be triggered by loss of beta2-adrenergic receptor signaling. |
