Abstract
Fibroblasts mediate acute wound healing and long-term tissue remodeling with scarring after tissue injury. Following myocardial infarction (MI), necrotized cardiomyocytes become replaced by secreted extracellular matrix proteins produced by fibroblasts. Dendritic cells (DCs) can migrate from the bone marrow to the infarct areas and infarct border areas to mediate collagen accumulation after MI. Trichostatin A (TSA) is known to regulate apoptosis and proliferation in fibroblasts and affect the functions of DCs under oxygen-glucose deprivation (OGD) conditions. In this study, we used label-free quantitative proteomics to investigate the effects of TSA and bone marrow-derived dendritic cells (BMDCs) on NIH3T3 fibroblasts under OGD conditions. The results showed that the fatty acid degradation pathway was significantly upregulated in NIH3T3 cells under OGD conditions and that the fatty acid synthesis pathway was significantly downregulated in NIH3T3 cells treated with conditioned media (CM) from BMDCs treated with TSA under OGD conditions [BMDCs-CM(TSA)]. In addition, BMDCs-CM(TSA) significantly decreased the levels of triglycerides and free fatty acids and mediated fatty acid metabolism-related proteins in NIH3T3 cells under OGD conditions. In summary, this proteomics analysis showed that TSA and BMDCs affect fatty acid metabolism in NIH3T3 cells under OGD conditions.