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. Author manuscript; available in PMC: 2009 Jul 15.
Published in final edited form as: Cardiovasc Res. 2008 Apr 25;79(2):341–351. doi: 10.1093/cvr/cvn104

Figure 6.

Figure 6

Inhibiting mitochondrial fission in sustained high glucose incubation prevents ROS overproduction and MPT. (A–D) Control cells show low levels of ROS in normal glucose conditions (A), and elevated ROS in the 48-hour high glucose incubation (B). ROS levels did not increase in H9c2 cells infected with Ad-DLP1-K38A in the 48-hour incubation in high glucose conditions (C). Scale bar: 20µm. Quantification of ethidium fluorescence indicates that ROS levels of Ad-DLP1-K38A-infected cells in high glucose conditions were similar to those in normal glucose incubation (D). Error bars represent SEM. ** indicates a statistically significant difference compared with the Control at p<0.01. (E) Co-Q assays for the MPT show that H9c2 cells infected with Ad-DLP1-K38A in high glucose conditions exhibited calcein levels similar to those of cells in normal glucose conditions. (F, G) Inhibition of mitochondrial fission in primary cells from cardiovascular system prevented the ROS increase in sustained high glucose conditions. Ad-DLP1-K38A infection decreased ROS levels in BAEC (F) and SMC (G) incubated for 48 hours in both 20 and 35mM glucose. Error bars represent SEM.