Mitomycin C modulates intracellular matrix metalloproteinase-9 expression and affects corneal fibroblast migration.

摘要: Abstract Mitomycin C (MMC) is often used to prevent postoperative corneal haze and subconjunctival fibrosis in ocular surgery. It also affects the motility viability of residual cells, including stromal cells. Extracellular matrix metalloproteinase-9 (MMP-9) contributes promotion cell movement macrophage cancer but intracellular role MMP-9 remained unclear. Herein, we illustrated novel MMC-suppressed migration using isolated human fibroblasts (HCFs). In HCFs, MMC enhanced at transcriptional protein levels. Using co-immunoprecipitation analysis, confirmed that association between inactive FAK/paxillin (PXN) complexes, i.e. PXN without phospho-tyrosine 118 (pY118) FAK 397 (pY397). To verify migration, its gene was directly from HCFs highly expressed by a lentivirus-based pseudovirus system with encephalomyocarditis virus (EMCV)-driven green fluorescent (GFP) as MMP-9-IG-versus IG-expressing Compared higher expression MMP-9-IG-expressing proliferated migrated more slowly. Phosphorylation Y397 both Y31 Y118 were significantly less HCFs. These suggested MMC-upregulated clutched FAK/PXN complexes focal adhesion sites form new “inactive” trimer, prohibited phosphorylation retarded fibroblast migration.