Research Paper Volume 12, Issue 23 pp 23684—23697
Hypoxia induces pulmonary artery smooth muscle dysfunction through mitochondrial fragmentation-mediated endoplasmic reticulum stress
Figure 7. Inhibition of mitochondrial fragmentation using Mdivi-1 improved pulmonary artery smooth muscle function in response to hypoxia in vivo. (A) Mdivi-1 treatment decreased Drp1 and Drp1 phosphorylation at serine 616 in PASMCs of hypoxic rats. Twenty micrograms of protein was loaded in each lane. (B, C) Mdivi-1 treatment decreased both mPAP and PVR in hypoxia rats. (D) Mdivi-1 treatment deceased ER stress as detected by CHOP in isolated endothelium-denuded pulmonary arteries from hypoxic rats. Twenty micrograms of protein was loaded in each lane. (E, F) Mdivi-1 treatment improved PE-induced vasoconstriction (E) and ACh/SNP-induced vasodilation (F) in isolated pulmonary arteries from hypoxic rats. *, p < 0.05, **, p < 0.01. n = 8.