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. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: J Cell Biochem. 2018 Aug 3;119(11):9394–9407. doi: 10.1002/jcb.27256

Fig. 6.

Fig. 6.

Respiratory control ratio (A) and mitochondrial membrane potential (ΔΨm, B) in non-injured and TBHP-injured RPTC expressing caPKCε or dnPKCε mutants of PKCε at 4 hours (A) and 4 and 24 hours following TBHP-induced injury. ΔΨm is expressed as the ratio of J-aggregate (red fluorescence) to monomeric form of JC-1 (green fluorescence). RPTC were subjected to adenoviral infection for 24 hours, the adenovirus was removed by aspirating media, and RPTC were incubated in fresh media for subsequent 24 hours prior to the exposure to TBHP. Results are the average ± S.E. of 6–9 independent experiments (RPTC isolations). Values with dissimilar superscripts are significantly different (p<0.05) from their respective controls and from each other.