Apoptosis of pro-B lymphocytes induced by NR4A1 activation in the presence of gingival fibroblast exosomes and TNFα, caspase 8, STAT3, and Akt pathways modulators.

There is a lack of data in the mainstream literature regarding the interactions between gingival fibroblasts, as a component of the local niche, and tumor precursors of B-lymphocytes. Although it is known that the development of tumors and tumor precursors depends on the local environment's characteristics. In order to experimentally evaluate the apoptosis of pro-B type lymphocytes, induced as a result of the known activation of orphan nuclear receptor 4A1 (NR4A1), through Cytosporone B (Csn-B, 10 μM), in the presence or absence of exosomes derived from gingival fibroblasts, we administered as a treatment: 1 μM R-7050 [functional inhibitor of tumor necrosis factor alpha (TNFα)], 1 μM Z-IETD-FMK (functional inhibitor of caspase 8), 1 μM GSK690693 (functional inhibitor of Akt 1∕2∕3 pathways) and, last but not least, 1 μM scutellarin [functional inhibitor of receptor activator of nuclear factor-kappa B ligand (RANKL)] and therefore of the signal transducer and activator of transcription 3 (STAT3) pathway.

Thapsigargin-induced endoplasmic reticulum stress is not accompanied by mitochondrial membrane potential dissipation in murine pro-B cells.

Unlabelled: There are almost no data concerning the involvement of endoplasmic reticulum stress (Ca2+ fluxes) in the apoptosis of the pro-B cell type Ba/F3. Thus, we aimed the characterization of thapsigargin-induced effects on Ba/F3 cells in vitro.

Material And Method: For some experiments Ba/F3 cells were treated with 1 microM thapsigargin for 24 hours.