An Angiotensin II Type 1 Receptor Blocker Prevents Renal Injury via Inhibition of the Notch Pathway in Ins2 Akita Diabetic Mice
Figure 3
Telmisartan suppressed the activation of the Notch signaling pathway through inhibition of the angiotensin II type 1 receptor. The mRNA expression of Hes1, one of the Notch target genes; transforming growth factor β (TGF-β); vascular endothelial growth factor-A (VEGF-A) were examined by reverse transcriptase-polymerase chain reaction. (a) The podocytes were stimulated with 10−6 M Angiotensin II (AII) for 24 to 48 h. The mRNA expression of Hes1 increased in the presence of AII and peaked at 24 h. On the other hand, 10−6 M telmisartan suppressed the AII-induced mRNA expression of Hes1 (upper panel). Quantification of the Hes1 mRNA expression compared to the internal control (β-actin) (lower panel). (b) The podocytes were treated with 10−6 M AII in the presence or absence of 10−8 M candesartan for 24 h. Candesartan also suppressed the AII-induced mRNA expression of Hes1. (c) AII increased the TGF-β mRNA by 2.5-fold within 12 h. Telmisartan (10−6 M) suppressed the expression of TGF-β significantly. (d) AII increased the VEGF-A expression by 2.0-fold. Telmisartan suppressed the expression of VEGF-A significantly. *.
