Research Article

Hyperglycemia Induces Endoplasmic Reticulum Stress in Atrial Cardiomyocytes, and Mitofusin-2 Downregulation Prevents Mitochondrial Dysfunction and Subsequent Cell Death

Figure 3

Mfn2 siRNA disrupts endoplasmic reticulum- (ER-) mitochondria tethering in tunicamycin- (TM-) injured HL-1 cells. (a) Changes in GRP78 and Mfn2 levels induced by TM were examined using Western blot analysis. The silencing efficiency of Mfn siRNA also shown in (a). (b) Quantification of GRP78 and Mfn2 protein level in (a). (c) Quantification of Mfn2 mRNA expression. (d) Ultrastructural changes in HL-1 cells (green stars depicting the mitochondria, white arrowheads depicting the endoplasmic reticulum). Transmission electron micrograph images (red arrowheads depicting the ER-mitochondria contacts) and measurements of the ER-mitochondria distance (e). Scale bar, top 1 μm, middle 2 μm, and bottom 500 nm. Data are , independent experiments, #, ANOVA with Bonferroni posttest.
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