| First Author | Anquetil T | Year | 2021 |
| Journal | EMBO Rep | Volume | 22 |
| Issue | 6 | Pages | e51299 |
| PubMed ID | 33880878 | Mgi Jnum | J:307096 |
| Mgi Id | MGI:6711928 | Doi | 10.15252/embr.202051299 |
| Citation | Anquetil T, et al. (2021) PI3KC2beta inactivation stabilizes VE-cadherin junctions and preserves vascular integrity. EMBO Rep :e51299 |
| abstractText | Endothelium protection is critical, because of the impact of vascular leakage and edema on pathological conditions such as brain ischemia. Whereas deficiency of class II phosphoinositide 3-kinase alpha (PI3KC2alpha) results in an increase in vascular permeability, we uncover a crucial role of the beta isoform (PI3KC2beta) in the loss of endothelial barrier integrity following injury. Here, we studied the role of PI3KC2beta in endothelial permeability and endosomal trafficking in vitro and in vivo in ischemic stroke. Mice with inactive PI3KC2beta showed protection against vascular permeability, edema, cerebral infarction, and deleterious inflammatory response. Loss of PI3KC2beta in human cerebral microvascular endothelial cells stabilized homotypic cell-cell junctions by increasing Rab11-dependent VE-cadherin recycling. These results identify PI3KC2beta as a potential new therapeutic target to prevent aggravating lesions following ischemic stroke. |
