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

Figure 1

High glucose induces ER stress and upregulates intracellular and mitochondrial Ca²⁺ levels. (a) Primary atrial myocytes under normal glucose (NG) or high glucose (HG) with or without 4-PBA for 24 hours. Quantification of GRP78 and CHOP mRNA expression. (b) Primary atrial myocytes under NG or HG with or without 4-PBA for 48 hours. GRP78 and CHOP protein level in atrial myocytes detected by Western blot analysis. (c) Quantification of GRP78 and CHOP protein level in (b). (d) Representative confocal microscopy images of fluorescence staining for Fluo-4 AM and DAPI. Scale bar, 20 μm. (e) Quantification of Fluo-4 AM fluorescence intensity in (d). (f) Representative confocal microscopy images of fluorescence staining for Rhod2 AM and MitoTracker Green. Scale bar, 20 μm. (g) Quantification of Rhod2 AM fluorescence intensity in (f). (h) MAM proteins such as IP₃R1, GRP75, VDAC1, and Mfn2 protein level in atrial myocytes detected by Western blot analysis. (i) Quantification of IP3R1, GRP75, VDAC1, and Mfn2 protein level in (h). Data are , independent experiments, , ^#, ANOVA with Bonferroni posttest.

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