Abstract: Objective Oxidative stress is the main cause of podocyte apoptosis, and accelerates the disease course of chronic kidney disease. However, the mechanism of podocyte apoptosis by oxidative stress remains elusive. Here we investigated the induction of oxidative stress in podocytes through the phosphorylation of p47^phox by smooth muscle 22 alpha (SM22α) to regulate angiotensinⅡ(AngII). Methods The expression of SM22α, p47^phox and other proteins in normal podocytes and podocytes stimulated with AngII were measured by quantitative real time PCR and western blot. Changes of p47phox expression was evaluated under the knockdown of SM22α expression. Results After the stimulation of AngII for 12 hours, SM22α mRNA in podocytes decreased significantly (t=2.215, P=0.041), while p47^phox mRNA increased significantly (t=3.955, P =0.025); the down-regulation of SM22α (t=2.215, P=0.041) prompted oxidative stress in podocytes and the oxidative stress reached the peak after 12 hours (t^DHE=2.547, P^DHE=0.042; t^TBA=3.689, P^TBA=0.022). Conclusion AngII induced the dysfunction of SM22α and the phosphorylation of SM22α activated p47^phox, which suggests that SM22α plays important role in the oxidative stress in podocytes.

Key words: Angiotensin Ⅱ, podocyte, SM22α, proteinuria, p47^phox