| First Author | Du Y | Year | 2023 |
| Journal | iScience | Volume | 26 |
| Issue | 3 | Pages | 106114 |
| PubMed ID | 36852280 | Mgi Jnum | J:352753 |
| Mgi Id | MGI:7441589 | Doi | 10.1016/j.isci.2023.106114 |
| Citation | Du Y, et al. (2023) Protein kinase A activation alleviates cataract formation via increased gap junction intercellular communication. iScience 26(3):106114 |
| abstractText | Cataract is the leading cause of blindness worldwide. Here, we reported a potential, effective therapeutic mean for cataract prevention and treatment. Gap junction communication, an important mechanism in maintaining lens transparency, is increased by protein kinase A (PKA). We found that PKA activation reduced cataracts induced by oxidative stress, increased gap junctions/hemichannels in connexin (Cx) 50, Cx46 or Cx50 and Cx46 co-expressing cells, and decreased reactive oxygen species (ROS) levels. However, ROS reduction was shown in wild-type, Cx46 and Cx50 knockout, but not in Cx46/Cx50 double KO lens. In addition, PKA activation protects lens fiber cell death induced by oxidative stress via hemichannel-mediated glutathione transport. Connexin deletion increased lens opacity induced by oxidative stress associated with reduction of anti-oxidative stress gene expression. Together, our results suggest that PKA activation through increased connexin channels in lens fiber cell decreases ROS levels and cell death, leading to alleviated cataracts. |
