Objective: Mitofusin2(Mfn2) is an important mitochondrial protein inmaintaining mitochondrial network and bioenergetics. Recently, Mfn2have beenreported to have a potential role in regulating cell proliferation, apoptosis, anddifferentiation in many cell types.Methods: In this study, we performed immunohistochemistry, pulmonary arterysmooth muscle cells (PASMCs) DNA analysis, proliferating cell nuclear antigenexpression and cell cycle analysis to determine the role of Mfn2in hypoxia-inducedpulmonary vascular remodeling.Results: Our results showed that Hypoxia promoted the proliferation of pulmonaryartery smooth muscle, including regulating more cells at G2/M+S phase, increasingproliferating cell nuclear antigen and Cyclin A expression, whereas all these effects ofhypoxia was suppressed after the cells were treated with siRNA against Mfn2. Ourresults also proved that PI3K/Akt signaling pathway was involved in Mfn2–inducedsmooth muscle cell proliferation.Conclusion: Thus, these results indicated that Mfn2mediated PASMCproliferation in hypoxic pulmonary hypertension via the PI3K/Akt signaling pathway. |