期刊
MOLECULAR MEDICINE REPORTS
卷 14, 期 5, 页码 4383-4390出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2016.5752
关键词
pulmonary arterial hypertension; hypoxia inducible factor-1 alpha; hypoxia inducible factor-1 beta; signaling pathway; lung
资金
- Collaborative Innovation and Platform Environment Construction Projects of Guangdong Province [2015A050502049]
- Natural Science Foundation of Guangdong Province [2015A030313520]
- Science and Technology Planning Project of Guangdong Province [2014A020212739]
- Traditional Chinese Medicine Bureau of Guangdong Province [20151259, 20161142]
- National Natural Science Foundation of China [81300035]
Pulmonary arterial hypertension (PAH) is characterized by endothelial dysfunction and structural remodeling of the pulmonary vasculature, mediated initially by reduced oxygen availability in the lungs. Hypoxia inducible factor (HIF), consisting of the functional subunit, HIF-1 alpha, and the constitutively expressed HIF-1 beta, is involved in the pathological processes associated with hypoxia. In the current study, the sequences of cDNAs and amino acids of HIF were characterized and analyzed using online bioinformatics tools. To further evaluate whether HIF accounts for the occurrence of PAH, the present study determine the expression and phosphorylation levels of HIF and its associated pathways, including extracellular signal-regulated kinase (Erk) 1/2 and phosphoinositide 3-kinase (PI3K)/Akt, in the lungs of patients with PAH by reverse transcription-quantitative polymerase chain reaction and western blotting. The mRNA expression levels of PI3K, Erk2, and HIF-1 alpha in the patients with PAH were significantly higher, compared with those in the control group, by 3.6-fold (P<0.01), 4.06-fold and 2.64-fold (P<0.05), respectively. No significant differences were found in the mRNA and protein levels of Akt between the two groups (P>0.05). The protein levels of phosphorylated (p-) Akt, Erk1/2, p-Erk1/2, HIF-1 alpha and HIF-1 beta were significantly increased by 5.89-, 0.5-, 0.59-, 1.46- and 0.92-fold, respectively, in the patients with PAH, compared with those in the controls group (P<0.01 for p-Akt, Erk1/2; P<0.05 for p-Erk1/2, HIF-1 alpha and HIF-1 beta) . These findings suggested that the mitogen-activated protein kinase and PI3K/Akt signaling pathways, and HIF-1 may perform a specific function in the pathogenesis of PAH.
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