Integration von Qualitätsdaten für Produktionsanlagen

In automatisierten Produktionsanlagen werden mehr und mehr Sensorsysteme eingesetzt, um die produzierte Qualität zu überwachen und auf Basis gesammelter Prozessdaten sicherzustellen. Die Heterogenität der an unterschiedlichen Stellen im Prozess integrierten Sensoren erfordert einen Ansatz zur einfachen Integration. Ziel der Integration ist die für verschiedene Rollen aufbereitete Qualitätssicht, die auch ein Feedback zur Fehlerdeduktion beinhaltet. In diesem Erfahrungsbericht wird der im Projekt BridgeIT entwickelte Ansatz zur syntaktischen und semantischen Integration von Qualitätsdaten vorgestellt. Der Ansatz ermöglicht insbesondere eine einfache Anbindung neuer Sensorsysteme

Nrf2-mediated fibroblast reprogramming drives cellular senescence by targeting the matrisome

Nrf2 is a key regulator of the antioxidant defense system, and pharmacological Nrf2 activation is a promising strategy for cancer prevention and promotion of tissue repair. Here we show, however, that activation of Nrf2 in fibroblasts induces cellular senescence. Using a combination of transcriptomics, matrix proteomics, chromatin immunoprecipitation and bioinformatics we demonstrate that fibroblasts with activated Nrf2 deposit a senescence-promoting matrix, with plasminogen activator inhibitor-1 being a key inducer of the senescence program. In vivo, activation of Nrf2 in fibroblasts promoted re-epithelialization of skin wounds, but also skin tumorigenesis. The pro-tumorigenic activity is of general relevance, since Nrf2 activation in skin fibroblasts induced the expression of genes characteristic for cancer-associated fibroblasts from different mouse and human tumors. Therefore, activated Nrf2 qualifies as a marker of the cancer-associated fibroblast phenotype. These data highlight the bright and the dark sides of Nrf2 and the need for time-controlled activation of this transcription factor

Serine protease 35 regulates the fibroblast matrisome in response to hyperosmotic stress

Hyperosmotic stress occurs in several diseases, but its long-term effects are largely unknown. We used sorbitol-treated human fibroblasts in 3D culture to study the consequences of hyperosmotic stress in the skin. Sorbitol regulated many genes, which help cells cope with the stress condition. The most robustly regulated gene encodes serine protease 35 (PRSS35). Its regulation by hyperosmotic stress was dependent on the kinases p38 and JNK and the transcription factors NFAT5 and ATF2. We identified different collagens and collagen-associated proteins as putative PRSS35 binding partners. This is functionally important because PRSS35 affected the extracellular matrix proteome, which limited cell proliferation. The in vivo relevance of these findings is reflected by the coexpression of PRSS35 and its binding partners in human skin wounds, where hyperosmotic stress occurs as a consequence of excessive water loss. These results identify PRSS35 as a key regulator of the matrisome under hyperosmotic stress conditions.ISSN:2375-254