Endometrosis in mares is characterized by inflammation, with continuous activity mainly of the profibrotic cytokine TGFβ. Other proinflammatory cytokines (IL-1, IL-6 and TNF-α) might impact on fibrosis. This aberrant signaling favors conversion of fibroblasts into myofibroblasts, exacerbating the expression of a-SMA, an imbalance of MMPs/TIMPs and uncontrolled deposition of extracellular matrix components. Also, miRNA deregulation impacts on gene expression controlling fibrosis. MicroRNA might be engulfed in extracellular vesicles (EV) secreted by fibrotic cells and induce the pathogenic phenotype in neighboring cells. We challenged endometrial fibroblasts in vitro with either TGFβ alone, combined with other cytokines (TGFβ + IL1 + IL6 + TNF -α; 10ng/ml each cytokine) or vehicle (DMEM, 1% FCS) for 24h. At time points zero, 24, 48 and 72h, cellular proteins were isolated for Western blot analysis and mRNA was converted to cDNA for RT-qPCR. Culture medium was also collected and EV separated by ultracentrifugation, quantified using NTA and Western blotting and their cargo offibrotic-related miRNAs was evaluated using the DDCT qPCR method; this was expressed in Fold Change (FC) with the vehicle group as the reference. Statistical analysis included ANOVA and Tukey posthoc, significance was set at p<0.05. Profibrotic genes aSMA, Col3A1/Col1a1, MMP9/TIMP1, MMP2/TIMP2 were upregulated in the treated groups, as well as phosphorylation of SMAD2 protein. Profibrotic miRNAs (miR17, 21 and 433) were upregulated, while anti-fibrotic miRNAs (miR26, 29a/b, 145,378 and 488) were downregulated in the treatment groups, but not in the vehicle control. TGFβ is sufficient for converting fibroblast to myofibroblast; however, the combined used of selected pro-inflammatory cytokines exacerbates the fibrotic phenotype. These findings may help to unravel the role of inflammation in the early stages of endometrial fibrosis in mares and also to develop cellular models in which to test anti-fibrotic drugs or therapeutic approaches. Funding: FONDECYT 1210349 and VRID 219.153.027-INV.