Basic & Clinical Medicine ›› 2018, Vol. 38 ›› Issue (6): 751-758.

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Endothelial progenitor cells with overexpressing angiotensin-converting enzyme 2 reduce monocrotaline-induced pulmonary arterial hypertension in rats

  

  • Received:2017-10-19 Revised:2018-01-26 Online:2018-06-05 Published:2018-05-25

Abstract: Objective To investigate the therapeutic effect of endothelial progenitor cells (EPCs) overexpressing angiotensin converting enzyme 2 (ACE2) on rat models of monocrotaline (MCT) induced pulmonary arterial hypertension (PAH). Methods EPCs were extracted, purified and identified from the very beginning. The lentivirus vector carrying ACE2 gene was infected with EPCs in order to prepare the ACE2- EPCs. Besides, the expression levels of ACE2 and proliferation as well as tube function of EPCs were detected before and after the transduction. The SD rat were randomly divided into control group, MCT induced pulmonary arterial hypertension group (PAH group), ACE2 transduction of endothelial progenitor cells group (lenti-ACE2-EPCs group) and endothelial progenitor cells group (EPCs group). The mean pulmonary artery pressure of rats (mPAP) and right ventricular hypertrophy index (RV/LV+S) were determined in the third week after the molding; the lung tissue specimens were stained with HE and the pulmonary arterial wall thickness index (TI) as well as area index (AI) were also calculated; The expression levels of ACE2 in lung tissue were detected by Western blot. Results The mPAP, RV/LV+S, TI and AI detected in PAH group in the third week after the molding were markedly lower than those in control group (P<0.01); The mPAP, RV/LV+S, TI and AI detected in lenti-ACE2-EPCs group in the third week after the molding were markedly lower than those in PAH group and EPCs group (P<0.01); The expression level of ACE2 in lung tissue of lenti-ACE2-EPCs group was significantly higher than that in PAH group (P<0.01); The mPAP, RV/LV+S, TI and AI detected in EPCs group in the third week after the molding were markedly lower than those in PAH group (P<0.01), while higher than that when compared with control group and lenti-ACE2-EPCs group (P<0.01). Conclusions ACE2 overexpressing in endothelial progenitor cells (EPCs) can effectively reduce the mean pulmonary arterial pressure in PAH rat models, and the therapeutic effect of ACE2-EPCs is generally better than that of EPCs.

Key words: Key words: pulmonary arterial hypertension, endothelial progenitor cells, angiotensin converting enzyme 2

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