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. 2017 May 31;313(2):C207–C218. doi: 10.1152/ajpcell.00241.2016

Fig. 4.

Fig. 4.

Effects of chronic hypoxia and ET-1 treatment on proliferation. ET-1 treatment significantly decreased colocalization of Ki-67 and SMαA in FH but not FN MCAs in both the inner and outer medial layers. In FN arteries, treatment with the PKC inhibitor chelerythrine was without effect in the outer layer but increased colocalization in the inner layer. In FH arteries, treatment with chelerythrine increased colocalization in both layers. Treatment with the CaMKII inhibitor KN93 was without effect compared with ET-1 alone in both layers of both normoxic and hypoxic arteries. Treatment with the p38 inhibitor SB203580 significantly decreased colocalization only in the outer layer of normoxic arteries. FN and FH values were significantly different for ET-1-treated arteries in the outer layer and were significantly different in the inner layer for all three groups treated with kinase inhibitors. Results are presented as means ± SE for n = 7–9 (FN) and n = 10–13 (FH). §P < 0.05, FN vs. FH. *P < 0.05, ET-1 vs. ET-1 with inhibitor treatments.