Research Paper Volume 12, Issue 23 pp 23684—23697
Hypoxia induces pulmonary artery smooth muscle dysfunction through mitochondrial fragmentation-mediated endoplasmic reticulum stress
Figure 3. Mitochondrial fragmentation enhanced ER stress in cultured PASMCs under hypoxia. (A) Mdivi-1 treatment decreased Drp1 and Drp1 phosphorylation at serine 616 in PASMCs under hypoxia. Twenty micrograms of protein was loaded for each lane. (B) Mdivi-1 treatment inhibited mitochondrial fragmentation in PASMCs under hypoxia. Scale bar, 20 μm. (C) Mdivi-1 treatment inhibited ER stress as evidenced by the decreased CHOP expression in PASMCs under hypoxia. Twenty micrograms of protein was loaded for each lane. (D) Mdivi-1 treatment improved PASMC function as evidenced by increased PE/SNP-induced MLC phosphorylation/dephosphorylation in PASMCs under hypoxia. Twenty micrograms of protein was loaded for each lane. *, p < 0.05, **, p < 0.01. n = 8.