| First Author | He T | Year | 2020 |
| Journal | Arch Biochem Biophys | Volume | 682 |
| Pages | 108286 | PubMed ID | 32007475 |
| Mgi Jnum | J:288854 | Mgi Id | MGI:6416358 |
| Doi | 10.1016/j.abb.2020.108286 | Citation | He T, et al. (2020) Notch signal deficiency alleviates hypertrophic scar formation after wound healing through the inhibition of inflammation. Arch Biochem Biophys 682:108286 |
| abstractText | Pathological scar is a common complication after wound healing. One of the most important factors that affects scar formation is inflammation. During this process, macrophages play a critical role in the wound healing process, as well as in scar formation. Notch signaling is reported to participate in inflammation and fibrosis; however, whether it affects scar formation is still unclear. In this study, RBP-J knockout mice, in which Notch signaling was down-regulated, and control mice were used, and a skin incision model was established. Sirius red staining and Masson staining suggested that RBP-J knockout could significantly reduce collagen sedimentation after wound healing. Western blot analysis and RT-PCR also confirmed the results. During wound healing, the expression of inflammatory cytokines and macrophage infiltration were decreased in RBP-J knockout mice. In vitro, it was also verified that RBP-J deficiency in macrophages effectively suppressed the expression of inflammatory cytokines and chemotaxis of macrophages after LPS stimulation. In conclusion, blocking Notch signaling in macrophages effectively alleviated scar formation by suppressing the inflammatory response and collagen sedimentation. |
