Fig. 5: MSCs suppress HG-induced endothelial inflammation by STC1-dependent mitochondrial dynamics remodeling. | Cell Death & Disease

Fig. 5: MSCs suppress HG-induced endothelial inflammation by STC1-dependent mitochondrial dynamics remodeling.

From: MSCs ameliorates hyperglycemia-induced endothelial injury through modulation of mitochondrial dynamics

Fig. 5: MSCs suppress HG-induced endothelial inflammation by STC1-dependent mitochondrial dynamics remodeling.The alternative text for this image may have been generated using AI.

A HUVECs were cocultured with MSCs transfected with scramble siRNA or with STC1 siRNA, mRNA expression of inflammatory adhesion molecules was analyzed by qPCR (n = 5 independent experiments). Data are shown as means ± SD. *P < 0.05. B, C Representative Western blots and densitometric analysis of protein levels of ICAM1 and VCAM1 in HUVECs from each group (n = 5 independent experiments). Data are shown as means ± SD. *P < 0.05. D, E Representative images and corresponding quantitation showed the adhesion of monocytes to the lawn of HUVECs (n = 5 independent experiments). Data are shown as means ± SD. *P < 0.05. F HUVECs were exposed to HG, and transfected with si-ERK1/2 or treated with rSTC1 and/or transfected with constitutively active ERK2 (ERK2-CA), mRNA expression of inflammatory adhesion molecules was analyzed by qPCR (n = 3 independent experiments). Data are shown as means ± SD. *P < 0.05. G, H Cells lysates were analyzed by Western blot analysis for the expression of ICAM1 and VCAM1, as illustrated (n = 5 independent experiments). Data are shown as means ± SD. *P < 0.05. I, J Representative images and corresponding quantitation show the adhesion of monocytes to the lawn of HUVECs (n = 5 independent experiments). Data are shown as means ± SD. *P < 0.05. Data were analyzed using one-way ANOVA with Tukey’s post hoc test.

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