2 research outputs found
Secretome of Mesenchymal Stromal Cells as a Possible Innovative Therapeutic Tool in Facial Nerve Injury Treatment
Facial nerve palsy is a serious neurological condition that strongly affects patient everyday life. Standard treatments provide insufficient improvement and are burdened with the risk of severe complications, e.g., facial synkinesis. Mesenchymal stromal cell-based therapies are a novel and extensively developed field which offers new treatment approaches with promising results in regards to the nervous tissue regeneration. The potential of mesenchymal stromal cells (MSCs) to aid the regeneration of damaged nerves has been demonstrated in several preclinical models, as well as in several clinical trials. However, therapies based on cell transplantation are difficult to standardize in the manner similar to that of routine clinical practices. On the other hand, treatments based on mesenchymal stromal cell secretome harness the proregenerative features of mesenchymal stromal cells but relay on a product with measurable parameters that can be put through standardization procedures and deliver a fully controllable end-product. Utilization of mesenchymal stromal cell secretome allows the controlled dosage and standardization of the components to maximize the therapeutic potential and ensure safety of the end-product
Interaction between Macrophages and Human Mesenchymal Stromal Cells Derived from Bone Marrow and Wharton’s Jelly—A Comparative Study
Despite intensive clinical research on the use of mesenchymal stromal cells (MSCs), further basic research in this field is still required. Herein, we compared human bone marrow MSCs (BM-MSCs, n = 6) and Wharton’s jelly MSCs (WJ-MSCs, n = 6) in their ability to interact with human primary macrophages. Evaluation of secretory potential revealed that under pro-inflammatory stimulation, WJ-MSCs secreted significantly more IL-6 than BM-MSCs (2-fold). This difference did not translate into the effect of MSCs on macrophages: both types of MSCs significantly directed M1-like macrophages toward the M2 phenotype (based on CD206 expression) to a similar extent. This observation was consistent both in flow cytometry analysis and immunocytochemical assessment. The effect of MSCs on macrophages was sustained when IL-6 signaling was blocked with Tocilizumab. Macrophages, regardless of polarization status, enhanced chemotaxis of both BM-MSCs and WJ-MSCs (p < 0.01; trans-well assay), with WJ-MSCs being significantly more responsive to M1-derived chemotactic signals than BM-MSCs. Furthermore, WJ-MSCs increased their motility (scratch assay) when exposed to macrophage-conditioned medium while BM-MSCs did not. These results indicate that although both BM-MSCs and WJ-MSCs have the ability to reciprocally interact with macrophages, the source of MSCs could slightly but significantly modify the response under clinical settings