| First Author | Liu L | Year | 2017 |
| Journal | PLoS One | Volume | 12 |
| Issue | 12 | Pages | e0190253 |
| PubMed ID | 29287085 | Mgi Jnum | J:257873 |
| Mgi Id | MGI:6112825 | Doi | 10.1371/journal.pone.0190253 |
| Citation | Liu L, et al. (2017) Loss of TLR4 in mouse Muller cells inhibits both MyD88-dependent and -independent signaling. PLoS One 12(12):e0190253 |
| abstractText | Muller cells are key to metabolic and ionic regulation in the retina. They also produce a number of inflammatory mediators and are significantly affected in diabetic retinopathy. To investigate the role of toll-like receptor 4 (TLR4) in retinal Muller cells, we crossed TLR4 floxed with PDGFRalpha-Cre mice to eliminate TLR4 in retinal Muller cells. We performed Western blotting and ELISA analyses to determine whether loss of TLR4 affected myeloid differentiation primary response protein (MyD88)-dependent or -independent signaling, leading to reduced levels of tumor necrosis factor alpha (TNFalpha) and interleukin 1 beta (IL1beta) in whole retinal lysates from the TLR4 floxed and TLR4-PDGFRalpha-Cre mice. Data show that TLR4-PDGFRalpha-Cre mice have reduced levels of both the MyD88-dependent and -independent signaling pathways. These studies confirm successful development of a Muller cell-specific TLR4 knockout mouse colony. These mice have reduced MyD88-dependent and -independent signaling pathway proteins, as well as reduced TNFalpha and IL1beta levels. These mice can be used to dissect TLR4 signaling in disorders affecting retinal Muller cells. |
