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. Author manuscript; available in PMC: 2021 Mar 29.
Published in final edited form as: Kidney Int. 2011 Jan 26;79(8):861–870. doi: 10.1038/ki.2010.527

Figure 5 |. Effect of heat shock protein 70 (Hsp70) on mitochondrial Bax translocation and survival in primary renal epithelial cells harvested from Hsp70−/− mice.

Figure 5 |

(a) Localization of active Bax (that is, 6A7 epitope exposed; shown in red) and mitochondria (using MitoTracker Green FM) in control (‘empty vector’) and Hsp70-expressing (‘Hsp70 lentivirus’) proximal tubule cells in primary culture at baseline and 6 h following 1 h of ATP depletion; colocalization of the two probes appears as an orange–yellow color; virtually no active Bax was detected at baseline; results are representative of six separate studies. (b) Effect of Hsp70 expression on survival after 1 h of ATP depletion and 6 h of recovery in primary proximal tubule cells harvested from Hsp70+/+ and Hsp70−/− mice in the presence of lentivirus virus containing either empty vector or human Hsp70 (Hsp70). *P<0.05; NS, not significant. Data are mean±s.e; n = 7; immunoblot analysis shows Hsp70 content in cell lysates.