Roles Of Heat Shock Protein 70 Toward Hypoxia-Inducible Factor 1 Alpha (Hif-1 Alpha) Blockade In Newborn Rats With Hypoxia-Induced Pulmonary Hypertension

The aim of the present study was to investigate the roles of adenovirus-mediated heat shock protein 70 (HSP70) in newborn rats with hypoxia-induced pulmonary hypertension (HPH). A total of 128 newborn rats were randomly divided into an HPH group (H) and control group (C), with 8 rats in each group. According to transfection solutions received, group H was subgrouped into three different groups: Group H1, which received saline, group H2, which received transfection of an empty virus, and group H3, which received transfection of HSP70 virus. Subsequently, pulmonary artery pressure (mPAP) was measured in all groups and levels of HSP70, hypoxia-inducible factor 1 alpha (HIF-1 alpha), endothelin-1 (ET-1), and inducible nitric oxide synthase (iNOS) were measured at different time points. mPAP in groups H1 and H2 at 3 days, 7 days, 10 days, and 14 days was significantly higher than in group C (P<0.05). Furthermore, immunohistochemical expression intensity of HSP70 in group H3 on days 3, 7, and 10 was significantly enhanced (P<0.05), compared to groups H1 and H2. However, expression of HIF-1 alpha, ET-1, and iNOS in group H3 was reduced (P<0.01). Intergroup comparisons of HSP70 expression determined that expression of HSP70 in group H3 was enhanced (P<0.05), however expression of HIF-1 alpha, ET-1, and iNOS was reduced (P<0.05), compared to groups H1 and H2. Results of current study demonstrate that expression of adenovirus-mediated HSP70 in newborn HPH rats may downregulate expression of HIF-1 alpha, ET-1, and iNOS, reducing mPAP. Therefore, adenovirus-mediated HSP70 may be developed as a novel therapeutic method of treating neonatal HPH.