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Published on: October 19, 2013
[Protective effects of heat shock protein 70 against hypoxic pulmonary hypertension in neonatal rats]
Le Wang1, Hai-Yan Wu, Ming-Xia Li
1Department of Neonatology, First Affiliated Hospital of Xinjiang Medical University, Ürümqi 830054, China. 2583051008@qq.com.
Insights
Heat shock protein 70 (HSP70) protects against hypoxic pulmonary hypertension (HPH) in neonatal rats. HSP70 therapy reduced pulmonary artery pressure and vascular remodeling, offering a potential new treatment for HPH.
Area of Science:
- Cardiovascular Research
- Neonatal Medicine
- Molecular Biology
Background:
- Hypoxic pulmonary hypertension (HPH) poses a significant threat to neonates.
- Understanding the molecular mechanisms underlying HPH is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the protective effects of heat shock protein 70 (HSP70) against HPH in a neonatal rat model.
- To evaluate HSP70's impact on pulmonary artery pressure and vascular remodeling.
Main Methods:
- Neonatal rats were divided into control, HPH model, empty virus, and HSP70-treated groups.
- HPH was induced, and interventions (saline, Ad-GFP, or Ad-HSP70) were administered.
- Pulmonary artery pressure, vascular structure, and protein expression (HSP70, HIF-1α, ET-1, iNOS) were assessed.
Main Results:
- HSP70 treatment significantly reduced mean pulmonary arterial pressure (mPAP) compared to HPH model and empty virus groups.
- HSP70 administration alleviated pulmonary vascular remodeling (MA% and MT%).
- HSP70 group showed increased HSP70 expression and decreased expression of HIF-1α, ET-1, and iNOS.
Conclusions:
- HSP70 transfection effectively increases HSP70 expression in lung tissue.
- HSP70 downregulates HIF-1α, ET-1, and iNOS, mitigating pulmonary vascular remodeling and reducing pulmonary artery pressure.
- HSP70 represents a promising therapeutic strategy for neonatal HPH.
Objective:
To investigate the protective effect of heat shock protein 70 (HSP70) against hypoxic pulmonary hypertension (HPH) in neonatal rats.
Methods:
A total of 128 neonatal rats were randomly divided into blank control group, HPH model group, empty virus group, and HSP70 group, with 32 rats in each group. Before the establishment of an HPH model, the rats in the blank control group and HPH model group were given caudal vein injection of 5 μL sterile saline, those in the empty virus group were given caudal vein injection of 5 μL Ad-GFP (1 010 PFU/mL), and those in the HSP70 group were given caudal vein injection of 5 μL Ad-HSP70 (1 010 PFU/mL). HPH model was prepared in the HPH model, empty virus, and HSP70 groups after transfection. At 3, 7, 10, and 14 days after model establishment, a multi-channel physiological recorder was used to record mean pulmonary arterial pressure (mPAP), optical and electron microscopes were used to observe the structure and remodeling parameters of pulmonary vessels, and Western blot was used to measure the protein expression of HSP70, hypoxia-inducible factor-1α (HIF-1α), endothelin-1 (ET-1), and inducible nitric oxide synthase (iNOS) in lung tissues.
Results:
At 3, 7, 10, and 14 days after model establishment, the HPH model group and the empty virus group had a significantly higher mPAP than the blank control group (P<0.05). On days 7 and 10 of hypoxia, the blank control group and the HSP70 group had significantly lower MA% and MT% than the HPH model group and the empty virus group (P<0.01); on day 14 of hypoxia, the HPH model group, empty virus group, and HSP70 group had similar MA% and MT% (P>0.05), but had significantly higher MA% and MT% than the blank control group (P<0.01). On days 3, 7 and 10 of hypoxia, the HSP70 group had significantly higher protein expression of HSP70 than the HPH model group, empty virus group, and blank control group (P<0.01); the HSP70 group had significantly lower expression of HIF-1α, ET-1, and iNOS than the HPH model group and the empty virus group (P<0.05) and similar expression of HIF-1α, ET-1, and iNOS as the blank control group (P>0.05).
Conclusions:
In neonatal rats with HPH, HSP70 transfection can increase the expression of HSP70 in lung tissues, downregulate the expression of HIF-1α, ET-1, and iNOS, alleviate pulmonary vascular remodeling, and reduce pulmonary artery pressure; therefore, it may become a new strategy for the treatment of HPH in neonates.
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