bFGF overexpression adipose derived mesenchymal stem cells improved the survival of pulmonary arterial endothelial cells via PI3k/Akt signaling pathway.
Wang P., Li J., Zhang C., Luo L., Ni S., Tang Z.
Animal Study, published in Int J Biochem Cell Biol (2019) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Int J Biochem Cell Biol (2019)
- Country
- Netherlands
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 31200125
- DOI
- 10.1016/j.biocel.2019.06.004
- Citations
- 13
Abstract (original English)
Pulmonary arterial hypertension (PAH) is characterized as pulmonary arterial endothelial dysfunction and endothelial cells over proliferation, therefore, the repair of pulmonary arterial endothelial cells has been a common goal in treating PAH. In the present study, human adipose derived mesenchymal stem cells (ASCs) were transfected with bFGF lentiviral vector and co-cultured with monocrotaline pyrrole treated human pulmonary arterial endothelial cells (HPAECs). The results showed that bFGF-ASCs improved the proliferation, viability and decreased the apoptosis of HPAECs, besides, improved PAH was observed in PAH rat models. Western blot analysis showed that the PI3k and p-Akt protein expression level increased in HPAECs, suggesting the activation of the PI3k/Akt signaling pathway. With the administration of LY294002, the bFGF induced HPAECs survival and PI3k/Akt signaling activation were successfully blocked. The present study demonstrated that bFGF transfected ASCs improved the survival of HPAECs by activating the PI3k/Akt pathway.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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