Fig. 2

Protective pathways activated in MIN6-cells by hTERT-MSC. a hTERT-MSC manufactured VEGF, IDO1, and TIMP-1 after interacting with STZ-injured MIN6-cells in DC and IDC. Comparatively, higher expression of these molecules were observed in DC. Control is considered as healthy hTERT-MSC without physical or indirect contact with MIN6-cells. b The presence of hTERT-MSC in both conditions DC and IDC restored Ins2 gene expression in STZ-injured MIN6-cells. Control is considered as healthy MIN6-cells without STZ and hTERT-MSC influence. c The phosphorylation of AKT and ERK in damaged MIN6-cells with representative nitrocellulose membrane in upper and quantification of expressions in the lower panel with control adjusted to a hundred percent. A similar amount of phosphorylated AKT was detected in DC (280.8 ± 36.40) and IDC (241.4 ± 50.29; p ≤ 0.341), but the higher p-ERK expression was noticed in DC (75.93 ± 8.2) compared to IDC (59.18 ± 2.4; p ≤ 0.05). d Next, we hypothesized that p-AKT and p-ERK stimulated by hTERT-MSC influenced BCL-2 and BAX signaling cascade. In fact, MIN6-cells showed an increased BCL2/BAX ratio in the presence of MSC indicating a cellular state of anti-apoptosis. The four experimental conditions were identical to those described in Fig. 1. IDC, indirect culture; DC, direct culture; hTERT-MSC, human telomerase reverse transcriptase mesenchymal stem cells; IDO1, indoleamine 2,3-dioxygenase 1; TIMP-1, TIMP metallopeptidase inhibitor 1; VEGF, vascular endothelial growth factor; Ins2, preproinsulin 2; ERK, extracellular signal-regulated kinases; AKT, protein kinase B; BCL-2, B cell lymphoma 2; BAX, BCL-2-associated X protein. Data represent the mean ± SEM, n = 4. Value considered significant at p ≤ 0.05, **p ≤ 0.01, and ***p ≤ 0.001