An Angiotensin II Type 1 Receptor Blocker Prevents Renal Injury via Inhibition of the Notch Pathway in Ins2 Akita Diabetic Mice
Figure 4
TGF-β and VEGF-A directly activated the Notch pathway. The podocytes were stimulated with 5 ng/mL transforming growth factor β (TGF-β) or 10 ng/mL vascular endothelial growth factor-A (VEGF-A) in the presence or absence of 10−6 M telmisartan. The mRNA expression of Hes1 was examined by reverse transcriptase-polymerase chain reaction. (a) TGF-β increased the expression of Hes1 irrespective of the presence or absence of telmisartan (upper panel). Quantification of Hes1 expression compared to the internal control (β-actin). TGF-β significantly increased the Hes1 expression within 2 h by 2.1-fold (lower panel). (b) VEGF-A increased the expression of Hes1 irrespective of the presence or absence of telmisartan (upper panel). Quantification of the Hes1 expression compared to the internal control (β-actin). VEGF-A significantly increased the Hes1 expression within 2 h by 1.6-fold (lower panel). *, n.s.: not significant.
