090 Therapeutic effect and molecular mechanism of oncostatin M-regulated senescence-autophagy crosstalk in psoriasis

Introduction: Psoriasis is a chronic, inflammatory skin disorder. Studies suggested dysregulations in cell programmed death keratinocytes may play role psoriasis. Previously, we found Oncostatin M (OSM) was overexpressed psoriatic lesions, and related to the expressions of cellular senescence autophagy markers. Therefore, hypothesized that OSM-regulated senescence-autophagy interaction maintenance stability barrier, thus participating pathogenesis Objectives: To explore molecular mechanism psoriasis from perspective regulated by OSM. Materials Methods: We utilized whole transcriptome sequencing, proteomics, immunohistochemistry, immunostaining for assessment clinical samples; CRISPR-Cas9 genome editing, non-viral transient lentivirus-mediated stable transfections, rtPCR, immunoprecipitation, Western blot investigation therapeutic effects OSM; protein-protein (PPI) online databases incorporating with dynamic transcriptomic proteomic inputs exploration OSM PPI network. Results: A significant level overexpression its receptor OSMR murine psoriasiform observed. report fusion protein targeting could bind effectively neutralize inhibitory function proliferation A375 human melanoma cells. The JAK-STAT pathway plays relationship between indicated. use well received model, reversal normalization skin, as an inhibition downstream phosphorylation STAT3 were also achieved. Conclusion: Our findings demonstrated regulatory keratinocytes, identified