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. Author manuscript; available in PMC: 2016 Mar 15.
Published in final edited form as: Growth Factors. 2015 Jun 26;33(3):192–199. doi: 10.3109/08977194.2015.1054990

Figure 4.

Figure 4

Inhibition of PKCδ and PKCζ by Compound 49b is mediated by IGFBP-3. Figures A, B show phosphorylation of PKCδ (A) and PKCζ(B) in control (Ctrl), diabetic (Diab), diabetic+Compound 49b (Diab+49b), diabetic+IGFBP-3 siRNA (Diab+Bp3 siRNA), diabetic+IGFBP-3 siRNA+Compound 49b (Diab+BP3 siRNA+49b) and diabetic+scrambled siRNA (Diab+scsiRNA) rat retina. Figure A demonstrates that IGFBP-3 siRNA was effective in reducing PKCδ phosphorylation. Figure B demonstrates that Compound 49b can decrease phosphorylation of PKCζ in the diabetic rat retina through increased IGFBP-3 levels. Figures C and D represent measurements of PKCδ (C) and PKCζ (D) in REC cultured in normal (NG) or high glucose (HG) and high glucose and treated with Compound 49b (HG +49b), high glucose, IGFBP-3 siRNA and Compound 49b (HG+Bp3 siRNA+49b) and high glucose with scrambled siRNA+49b (HG+Sc+49b). *p<0.05 versus NG or control, #p<0.05 versus HG or diabetes, $p<0.05 versus HG+49b or Diab+49b. N=5–6 for rat retina and N=4 for cell work.