miR-22-3p通过靶向AIFM1调控低氧诱导的肺动脉平滑肌 细胞线粒体稳态和凋亡

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【中图分类号】R473.72

【文献标志码】A

MiR-22-3p regulates hypoxia-induced mitochondrial homeostasis and apoptosis of pulmonary artery smooth muscle cells by targeting apoptosis-inducing factor，mitochondrion-associated 1

Xiang Yujing，Tang Huting，An Yong

（DepartmentofCardiothoracicSurgery，Children's HospitalofChongqing MedicalUniversity，National Clinical Re

search Centerfor Child Health andDisorders，MinistryofEducation KeyLaboratoryofChild Development and Disorders，Chongqing Key Laboratory of Structural Birth Defect and Reconstruction）

【AbstractOetiveTivesigatethectof-3pdaoposisdcinctorocondriosocatedo mitochondrial homeostasis and apoptosis of pulmonaryarterysmoth musclecels（PASMCs）underhypoxicconditions byestablishing aninvitro modelfpulmonary hypertension（PAH）.Methods：ASMCswereculturedunderhypoxicconditions toestablishaniitro modelofPAH，andtheexpresiolevelsofAIFM1andiR-22-3pwereupregulatdordowreglated.Reverse rascriptioquaiativepolymerasechainreaction（RT-qPCR）and Western bloting wereused to measurethe expresionlevelsofAIFM1，miR-22-3p， and cleaved cysteine-aspartic protease-3（Cleaved Caspase-3）. cell counting kit-8（CCK- 8 ）assay was used to measure the proliferativeactivityofcelsandfcometryassedtoeasrecelloptosis.ochondrialsuperoideinatoritoOX）adeno inetriphosphate（AT）assykitswereusedtoobservemitochondrialfunctionanddynamics，andMito-TrackerRedCMXRos（itoTracker）wasused tomeasure the change in mitochondrial circumference.Dual-luciferase reporter assay was used to validate the interaction between AIFM1and miR-22-3p.Results：Hypoxia increased the contentof mitochondrial ROS，reduced the level of ATP，promoted mitochondrial fission，and reduced cell apoptosisin PASMCs.AIFM1 overexpression improved mitochondrial homeostasisand increased cell apoptosis，while miR-22-3p negatively regulatedAIFM1 and reversedtheeffectof AIFM1 overexpression. Conclusion：This study showsthatmiR-22-3penhancesmitochon

drialhomeostasisoleratiodpotosisioxiiuedsygeting，ichrovdesotetialial basis for the prevention and treatment of PAH.

【Key words】pulmonary arterial hypertension ; mitochondrial homeostasis;apoptosis

体外肺动脉高压（pulmonaryarterialhyperten-sion，PAH）是以肺血管明显重构和肺血管负荷逐渐增加，进而导致右心室肥厚和重构为特征的疾病。（剩余17068字）