| First Author | Lappas M | Year | 2018 |
| Journal | Mol Cell Endocrinol | Volume | 473 |
| Pages | 61-71 | PubMed ID | 29330113 |
| Mgi Jnum | J:265868 | Mgi Id | MGI:6205281 |
| Doi | 10.1016/j.mce.2018.01.003 | Citation | Lappas M (2018) Runt-related transcription factor 1 (RUNX1) deficiency attenuates inflammation-induced pro-inflammatory and pro-labour mediators in myometrium. Mol Cell Endocrinol 473:61-71 |
| abstractText | Identifying new targets that regulate myometrial activation are required to develop effective treatments to stop preterm labor. Inflammation, which can be induced by sterile or infective insults, plays a role in initiating and maintaining uterine contractions. Several high throughput transcription screening studies have identified an upregulation of runt-related transcription factor 1 (RUNX1) mRNA expression in myometrium with labor. The role of RUNX1 in labor, however, is not known. We report increased RUNX1 during late gestation which was further augmented in labor, suggesting that RUNX1 may be involved in the transition of the myometrium from a quiescent into a contractile state in preparation for labor. By inhibiting the expression of RUNX1, we have established that RUNX1 induces the expression of pro-inflammatory cytokines, chemokines, adhesion molecules, contraction-associated proteins OXR and PTGFR, the uterotonic PGF2alpha, and the ECM remodelling enzyme MMP9. Targeting RUNX1 may be a novel approach to prevent preterm labor. |
